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Study · Animal study (in vivo) · mouse · 2025

13 results

Szeto-Schiller 31 eases acute lung injury in neonatal mice with acute respiratory distress syndrome by mediating TXNIP expression and NLRP3 inflammasome activation.

Zhu M, Song L, Wei Y, Hong F, Lu Y, Ji J, Yan Y

Translational pediatrics28 Jul 2025Cited by 2 (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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study13

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with ARDS, SS‑31 treatment ameliorated histopathological changes in the lungs.

    In plain wordsIn newborn mice with ARDS, SS‑31 improved lung tissue damage.

    Outcome
    DecreaseLung histopathological changes
    Study

    mousen: not reported in source

    neonatal ARDS mice
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistently, SS-31 treatment ameliorated histopathological changes and oedema in the lungs of neonatal ARDS mice, accompanied by improved alveolar capillary barrier integrity as well as reduced OxS, inflammation, and apoptosis.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with ARDS, SS‑31 treatment ameliorated oedema in the lungs.

    In plain wordsIn newborn mice with ARDS, SS‑31 reduced lung swelling.

    Outcome
    DecreaseLung oedema
    Study

    mousen: not reported in source

    neonatal ARDS mice
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistently, SS-31 treatment ameliorated histopathological changes and oedema in the lungs of neonatal ARDS mice, accompanied by improved alveolar capillary barrier integrity as well as reduced OxS, inflammation, and apoptosis.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with ARDS, SS‑31 treatment improved alveolar capillary barrier integrity.

    In plain wordsIn newborn mice with ARDS, SS‑31 improved the lung barrier between air sacs and blood vessels.

    Outcome
    IncreaseAlveolar capillary barrier integrity
    Study

    mousen: not reported in source

    neonatal ARDS mice
    Outcome group
    Vascular function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistently, SS-31 treatment ameliorated histopathological changes and oedema in the lungs of neonatal ARDS mice, accompanied by improved alveolar capillary barrier integrity as well as reduced OxS, inflammation, and apoptosis.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with ARDS, SS‑31 treatment reduced oxidative stress.

    In plain wordsIn newborn mice with ARDS, SS‑31 lowered oxidative stress.

    Outcome
    DecreaseOxidative stress in lungs
    Study

    mousen: not reported in source

    neonatal ARDS mice
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistently, SS-31 treatment ameliorated histopathological changes and oedema in the lungs of neonatal ARDS mice, accompanied by improved alveolar capillary barrier integrity as well as reduced OxS, inflammation, and apoptosis.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with ARDS, SS‑31 treatment reduced inflammation.

    In plain wordsIn newborn mice with ARDS, SS‑31 lowered inflammation.

    Outcome
    DecreaseInflammation in lungs
    Study

    mousen: not reported in source

    neonatal ARDS mice
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistently, SS-31 treatment ameliorated histopathological changes and oedema in the lungs of neonatal ARDS mice, accompanied by improved alveolar capillary barrier integrity as well as reduced OxS, inflammation, and apoptosis.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with ARDS, SS‑31 treatment reduced apoptosis.

    In plain wordsIn newborn mice with ARDS, SS‑31 lowered cell death.

    Outcome
    DecreaseApoptosis in lungs
    Study

    mousen: not reported in source

    neonatal ARDS mice
    Outcome group
    Cell viability and death · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistently, SS-31 treatment ameliorated histopathological changes and oedema in the lungs of neonatal ARDS mice, accompanied by improved alveolar capillary barrier integrity as well as reduced OxS, inflammation, and apoptosis.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  7. 07AnimalAnimal study (in vivo)Mechanism

    In ARDS animal models, SS‑31 treatment repressed TXNIP and NLRP3 protein levels.

    In plain wordsIn mice with ARDS, SS‑31 lowered the TXNIP and NLRP3 proteins.

    Outcome
    DecreaseTXNIP and NLRP3 protein levels in ARDS animals
    Study

    mousen: not reported in source

    neonatal ARDS mice
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Interestingly, SS-31 treatment repressed TXNIP and NLRP3 protein levels in ARDS cells and animal models.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  8. 08LabIn vitro (cells)Efficacy outcome

    In LPS-induced human lung microvascular cells, SS‑31 mitigated oxidative stress.

    In plain wordsIn lab tests on human lung cells, SS‑31 reduced oxidative stress caused by LPS.

    Outcome
    DecreaseOxidative stress injury in HLMVECs
    Study

    humann: not reported in source

    LPS-induced HLMVECs
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 treatment mitigated LPS-induced OxS, apoptosis, vascular permeability, and inflammatory response in HLMVECs.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  9. 09LabIn vitro (cells)Efficacy outcome

    In LPS-induced human lung microvascular cells, SS‑31 mitigated apoptosis.

    In plain wordsIn lab tests on human lung cells, SS‑31 reduced cell death caused by LPS.

    Outcome
    DecreaseApoptosis in HLMVECs
    Study

    humann: not reported in source

    LPS-induced HLMVECs
    Outcome group
    Cell viability and death · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 treatment mitigated LPS-induced OxS, apoptosis, vascular permeability, and inflammatory response in HLMVECs.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  10. 10LabIn vitro (cells)Efficacy outcome

    In LPS-induced human lung microvascular cells, SS‑31 mitigated vascular permeability.

    In plain wordsIn lab tests on human lung cells, SS‑31 reduced leakiness caused by LPS.

    Outcome
    DecreaseVascular permeability in HLMVECs
    Study

    humann: not reported in source

    LPS-induced HLMVECs
    Outcome group
    Vascular function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 treatment mitigated LPS-induced OxS, apoptosis, vascular permeability, and inflammatory response in HLMVECs.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  11. 11LabIn vitro (cells)Efficacy outcome

    In LPS-induced human lung microvascular cells, SS‑31 mitigated the inflammatory response.

    In plain wordsIn lab tests on human lung cells, SS‑31 reduced the inflammatory response caused by LPS.

    Outcome
    DecreaseInflammatory response in HLMVECs
    Study

    humann: not reported in source

    LPS-induced HLMVECs
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 treatment mitigated LPS-induced OxS, apoptosis, vascular permeability, and inflammatory response in HLMVECs.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated
  12. 12LabIn vitro (cells)Mechanism

    In ARDS cell models, SS‑31 treatment repressed TXNIP and NLRP3 protein levels.

    In plain wordsIn lab tests on ARDS cells, SS‑31 lowered the TXNIP and NLRP3 proteins.

    Outcome
    DecreaseTXNIP and NLRP3 protein levels in ARDS cells
    Study

    humann: not reported in source

    ARDS cells
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Interestingly, SS-31 treatment repressed TXNIP and NLRP3 protein levels in ARDS cells and animal models.
    1 context sentence
    Summary · context
    The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated

Studies that did not test the peptide alone1

In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Elamipretide (SS-31).

  1. 13Computer modelNot a test of Elamipretide (SS-31) aloneIn silicoMechanism

    A search of the STITCH chemical-interaction database indicated that SS‑31 works by mediating TXNIP expression.

    In plain wordsIn a computer database search, SS‑31 was linked to the TXNIP protein. This is a prediction, not a test in living cells.

    Outcome
    Not applicableSS-31 link to TXNIP expression in a chemical-interaction database
    Study

    n: not reported in source

    STITCH database search
    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Using the Search Tool for Interactions of Chemicals (STITCH) database, SS-31 was found to work via mediating TXNIP expression.

    In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

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

    10 Oct 2026, 08:19 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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