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Study · Animal study (in vivo) · mouse · 2016

29 results

Mitochondria-targeted peptide SS-31 attenuates renal injury via an antioxidant effect in diabetic nephropathy.

Hou Y, Li S, Wu M, Wei J, Ren Y, Du C, Wu H, Han C, Duan H, Shi Y

American journal of physiology. Renal physiology30 Dec 2015Cited by 108 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study29

29 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In diabetic mice, SS‑31 alleviated proteinuria.

    In plain wordsIn diabetic mice, SS‑31 reduced protein loss in urine, a sign of kidney injury.

    Outcome
    DecreaseProteinuria
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    The diabetic mice treated with SS-31 had alleviated proteinuria, urinary 8-hydroxy-2-deoxyguanosine level, glomerular hypertrophy, and accumulation of renal fibronectin and collagen IV.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 lowered urinary 8-hydroxy-2-deoxyguanosine level.

    In plain wordsIn diabetic mice, SS‑31 lowered a urine marker of oxidative damage.

    Outcome
    DecreaseUrinary 8-hydroxy-2-deoxyguanosine
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    The diabetic mice treated with SS-31 had alleviated proteinuria, urinary 8-hydroxy-2-deoxyguanosine level, glomerular hypertrophy, and accumulation of renal fibronectin and collagen IV.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In diabetic mice, SS‑31 alleviated glomerular hypertrophy.

    In plain wordsIn diabetic mice, SS‑31 reduced enlargement of the kidney's filtering units.

    Outcome
    DecreaseGlomerular hypertrophy
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    The diabetic mice treated with SS-31 had alleviated proteinuria, urinary 8-hydroxy-2-deoxyguanosine level, glomerular hypertrophy, and accumulation of renal fibronectin and collagen IV.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 alleviated accumulation of renal fibronectin.

    In plain wordsIn diabetic mice, SS‑31 reduced build-up of a scar-related protein, fibronectin, in the kidney.

    Outcome
    DecreaseRenal fibronectin accumulation
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Lung injury and fibrosis · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    The diabetic mice treated with SS-31 had alleviated proteinuria, urinary 8-hydroxy-2-deoxyguanosine level, glomerular hypertrophy, and accumulation of renal fibronectin and collagen IV.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 alleviated accumulation of renal collagen IV.

    In plain wordsIn diabetic mice, SS‑31 reduced build-up of collagen IV in the kidney.

    Outcome
    DecreaseRenal collagen IV accumulation
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Lung injury and fibrosis · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    The diabetic mice treated with SS-31 had alleviated proteinuria, urinary 8-hydroxy-2-deoxyguanosine level, glomerular hypertrophy, and accumulation of renal fibronectin and collagen IV.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 attenuated renal cell apoptosis.

    In plain wordsIn diabetic mice, SS‑31 reduced kidney cell death.

    Outcome
    DecreaseRenal cell apoptosis
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Cell viability and death · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    SS-31 attenuated renal cell apoptosis and expression of Bax and reversed the expression of Bcl-2 in diabetic mice kidneys.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 attenuated expression of Bax in the kidney.

    In plain wordsIn diabetic mice, SS‑31 lowered kidney levels of Bax, a cell-death protein.

    Outcome
    DecreaseRenal Bax expression
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Cell viability and death · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    SS-31 attenuated renal cell apoptosis and expression of Bax and reversed the expression of Bcl-2 in diabetic mice kidneys.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 reversed the diabetes-related change in Bcl-2 expression in the kidney.

    In plain wordsIn diabetic mice, SS‑31 reversed the diabetes-related change in kidney Bcl-2, a cell-survival protein.

    Outcome
    Direction not reportedRenal Bcl-2 expression
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Cell viability and death · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    SS-31 attenuated renal cell apoptosis and expression of Bax and reversed the expression of Bcl-2 in diabetic mice kidneys.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 inhibited expression of TGF-β1 in the kidney.

    In plain wordsIn diabetic mice, SS‑31 lowered kidney levels of TGF-β1, a scarring signal.

    Outcome
    DecreaseRenal TGF-β1 expression
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Lung injury and fibrosis · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Furthermore, SS-31 inhibited expression of transforming-growth factor (TGF)-β1, Nox4, and thioredoxin-interacting protein (TXNIP), as well as activation of p38 MAPK and CREB and NADPH oxidase activity in diabetic kidneys.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  10. 10AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 inhibited expression of Nox4 in the kidney.

    In plain wordsIn diabetic mice, SS‑31 lowered kidney levels of Nox4, an enzyme that makes reactive oxygen.

    Outcome
    DecreaseRenal Nox4 expression
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Furthermore, SS-31 inhibited expression of transforming-growth factor (TGF)-β1, Nox4, and thioredoxin-interacting protein (TXNIP), as well as activation of p38 MAPK and CREB and NADPH oxidase activity in diabetic kidneys.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  11. 11AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 inhibited expression of thioredoxin-interacting protein in the kidney.

    In plain wordsIn diabetic mice, SS‑31 lowered kidney levels of TXNIP, an oxidative stress protein.

    Outcome
    DecreaseRenal TXNIP expression
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Furthermore, SS-31 inhibited expression of transforming-growth factor (TGF)-β1, Nox4, and thioredoxin-interacting protein (TXNIP), as well as activation of p38 MAPK and CREB and NADPH oxidase activity in diabetic kidneys.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  12. 12AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 inhibited activation of p38 MAPK in the kidney.

    In plain wordsIn diabetic mice, SS‑31 reduced activation of a stress-signaling protein, p38 MAPK, in the kidney.

    Outcome
    DecreaseRenal p38 MAPK activation
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Furthermore, SS-31 inhibited expression of transforming-growth factor (TGF)-β1, Nox4, and thioredoxin-interacting protein (TXNIP), as well as activation of p38 MAPK and CREB and NADPH oxidase activity in diabetic kidneys.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  13. 13AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 inhibited activation of CREB in the kidney.

    In plain wordsIn diabetic mice, SS‑31 reduced activation of the signaling protein CREB in the kidney.

    Outcome
    DecreaseRenal CREB activation
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Furthermore, SS-31 inhibited expression of transforming-growth factor (TGF)-β1, Nox4, and thioredoxin-interacting protein (TXNIP), as well as activation of p38 MAPK and CREB and NADPH oxidase activity in diabetic kidneys.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  14. 14AnimalAnimal study (in vivo)Mechanism

    In diabetic mice, SS‑31 inhibited NADPH oxidase activity in the kidney.

    In plain wordsIn diabetic mice, SS‑31 lowered activity of NADPH oxidase, an enzyme that makes reactive oxygen, in the kidney.

    Outcome
    DecreaseRenal NADPH oxidase activity
    Study

    mousen: not reported in source

    Uninephrectomy and streptozotocin diabetic nephropathy
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated · intraperitoneal · 8 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Furthermore, SS-31 inhibited expression of transforming-growth factor (TGF)-β1, Nox4, and thioredoxin-interacting protein (TXNIP), as well as activation of p38 MAPK and CREB and NADPH oxidase activity in diabetic kidneys.
    2 context sentences
    Summary · context
    CD-1 mice underwent uninephrectomy and streptozotocin treatment prior to receiving daily intraperitoneal injection of SS-31 for 8 wk.
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  15. 15LabIn vitro (cells)Mechanism

    In mouse mesangial cells exposed to high glucose, SS‑31 inhibited reactive oxygen species generation.

    In plain wordsIn cells, SS‑31 reduced reactive oxygen production caused by high glucose.

    Outcome
    DecreaseROS generation under high glucose
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro experiments using MMCs revealed that SS-31 inhibited HG-mediated ROS generation
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  16. 16LabIn vitro (cells)Mechanism

    In mouse mesangial cells exposed to high glucose, SS‑31 inhibited apoptosis.

    In plain wordsIn cells, SS‑31 reduced cell death caused by high glucose.

    Outcome
    DecreaseApoptosis under high glucose
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Cell viability and death · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro experiments using MMCs revealed that SS-31 inhibited HG-mediated ROS generation, apoptosis, expression of cleaved caspase-3, Bax/Bcl-2 ratio, and cytochrome c (cyt c) release from mitochondria.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  17. 17LabIn vitro (cells)Mechanism

    In mouse mesangial cells exposed to high glucose, SS‑31 inhibited expression of cleaved caspase-3.

    In plain wordsIn cells, SS‑31 lowered a cell-death marker, cleaved caspase-3, raised by high glucose.

    Outcome
    DecreaseCleaved caspase-3 expression
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Cell viability and death · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro experiments using MMCs revealed that SS-31 inhibited HG-mediated ROS generation, apoptosis, expression of cleaved caspase-3, Bax/Bcl-2 ratio, and cytochrome c (cyt c) release from mitochondria.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  18. 18LabIn vitro (cells)Mechanism

    In mouse mesangial cells exposed to high glucose, SS‑31 inhibited the Bax/Bcl-2 ratio.

    In plain wordsIn cells, SS‑31 lowered the Bax/Bcl-2 ratio, a cell-death balance marker, raised by high glucose.

    Outcome
    DecreaseBax/Bcl-2 ratio
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Cell viability and death · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro experiments using MMCs revealed that SS-31 inhibited HG-mediated ROS generation, apoptosis, expression of cleaved caspase-3, Bax/Bcl-2 ratio, and cytochrome c (cyt c) release from mitochondria.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  19. 19LabIn vitro (cells)Mechanism

    In mouse mesangial cells exposed to high glucose, SS‑31 inhibited cytochrome c release from mitochondria.

    In plain wordsIn cells, SS‑31 reduced release of cytochrome c from mitochondria caused by high glucose.

    Outcome
    DecreaseCytochrome c release from mitochondria
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Cell viability and death · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro experiments using MMCs revealed that SS-31 inhibited HG-mediated ROS generation, apoptosis, expression of cleaved caspase-3, Bax/Bcl-2 ratio, and cytochrome c (cyt c) release from mitochondria.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  20. 20LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 normalized the alteration in mitochondrial potential.

    In plain wordsIn cells, SS‑31 normalized a change in mitochondrial potential caused by high glucose.

    Outcome
    Direction not reportedMitochondrial potential (ΔΨm)
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 normalized mitochondrial potential (ΔΨm) and ATP alterations
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  21. 21LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 normalized the alteration in ATP.

    In plain wordsIn cells, SS‑31 normalized a change in ATP caused by high glucose.

    Outcome
    Direction not reportedATP level
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 normalized mitochondrial potential (ΔΨm) and ATP alterations
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  22. 22LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 inhibited expression of TGF-β1.

    In plain wordsIn cells, SS‑31 lowered levels of TGF-β1, a scarring signal, under high glucose.

    Outcome
    DecreaseTGF-β1 expression in mesangial cells
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Lung injury and fibrosis · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and inhibited the expression of TGF-β1, Nox4, and TXNIP, as well as activation of p38 MAPK and CREB and NADPH oxidase activity in MMCs under HG conditions.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  23. 23LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 inhibited expression of Nox4.

    In plain wordsIn cells, SS‑31 lowered Nox4, an enzyme that makes reactive oxygen, under high glucose.

    Outcome
    DecreaseNox4 expression in mesangial cells
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and inhibited the expression of TGF-β1, Nox4, and TXNIP, as well as activation of p38 MAPK and CREB and NADPH oxidase activity in MMCs under HG conditions.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  24. 24LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 inhibited expression of TXNIP.

    In plain wordsIn cells, SS‑31 lowered TXNIP, an oxidative stress protein, under high glucose.

    Outcome
    DecreaseTXNIP expression in mesangial cells
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and inhibited the expression of TGF-β1, Nox4, and TXNIP, as well as activation of p38 MAPK and CREB and NADPH oxidase activity in MMCs under HG conditions.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  25. 25LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 inhibited activation of p38 MAPK.

    In plain wordsIn cells, SS‑31 reduced activation of the stress-signaling protein p38 MAPK under high glucose.

    Outcome
    Decreasep38 MAPK activation in mesangial cells
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and inhibited the expression of TGF-β1, Nox4, and TXNIP, as well as activation of p38 MAPK and CREB and NADPH oxidase activity in MMCs under HG conditions.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  26. 26LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 inhibited activation of CREB.

    In plain wordsIn cells, SS‑31 reduced activation of the signaling protein CREB under high glucose.

    Outcome
    DecreaseCREB activation in mesangial cells
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and inhibited the expression of TGF-β1, Nox4, and TXNIP, as well as activation of p38 MAPK and CREB and NADPH oxidase activity in MMCs under HG conditions.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  27. 27LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 inhibited NADPH oxidase activity.

    In plain wordsIn cells, SS‑31 lowered NADPH oxidase activity, a source of reactive oxygen, under high glucose.

    Outcome
    DecreaseNADPH oxidase activity in mesangial cells
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and inhibited the expression of TGF-β1, Nox4, and TXNIP, as well as activation of p38 MAPK and CREB and NADPH oxidase activity in MMCs under HG conditions.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  28. 28LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 reversed the reduction in thioredoxin biologic activity.

    In plain wordsIn cells, SS‑31 reversed a high-glucose drop in the activity of thioredoxin, an antioxidant protein.

    Outcome
    IncreaseThioredoxin biologic activity
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 treatment also could reverse the reduction of thioredoxin (TRX) biologic activity and upregulate expression of thioredoxin 2 (TRX2) in MMCs under HG conditions.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.
  29. 29LabIn vitro (cells)Mechanism

    In mouse mesangial cells under high glucose, SS‑31 upregulated expression of thioredoxin 2.

    In plain wordsIn cells, SS‑31 raised levels of thioredoxin 2, an antioxidant protein, under high glucose.

    Outcome
    IncreaseThioredoxin 2 expression
    Study

    mousen: not reported in source

    Mouse mesangial cells under high glucose
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 treatment also could reverse the reduction of thioredoxin (TRX) biologic activity and upregulate expression of thioredoxin 2 (TRX2) in MMCs under HG conditions.
    1 context sentence
    Summary · context
    Here, we investigated the effect and molecular mechanism of mitochondria-targeted antioxidant peptide SS-31 on injuries in diabetic kidneys and mouse mesangial cells (MMCs) exposed to high-glucose (HG) ambience.

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Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    9 Oct 2026, 18:17 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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