Skip to content

Study · Animal study (in vivo) · mouse · 2026

7 results

Cuproptosis of bronchial epithelial cells triggers airway remodeling in chronic asthma.

Wang M, Liu C, Li Z, Wang Y, Li Y, Pei F

Scientific reports13 Jan 2026

PMID41530300 (opens in a new tab)PMCIDPMC12868725 (opens in a new tab)DOI10.1038/s41598-025-34574-3 (opens in a new tab)PepBankPUB-41530300
Read at sourcePubMedAsk about this study
Jump to 7 results

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 study7

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mice with OVA-induced chronic asthma, SS‑31 substantially inhibited the rise in cuproptosis markers.

    In plain wordsIn mice with chronic asthma, SS‑31 reduced signs of a copper-linked cell death process.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCuproptosis markers (Cu2+ in BALF, FDX-1, LIAS, DLAT)
    Study

    mousen: not reported in source

    OVA-induced chronic asthma
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, a cuproptosis blocker, the mitochondrion-targeted antioxidant, Szeto-Schiller (SS)-31, substantially inhibited the above mentioned processes.
    3 context sentences
    Summary · context
    Cuproptosis increased after repetitive OVA exposure in chronic asthmatic mice, evidenced by increased Cu2+ levels in bronchoalveolar lavage fluid (BALF) and increased protein expression of cuproptosis-related genes (FDX-1, LIAS, and DLAT)
    Summary · context
    Repetitive OVA exposure was used to establish a mouse model of chronic asthma.
    Summary · context
    The human bronchial epithelial cell line BEAS-2B (BEAS-2B cells) was incubated with recombinant human IL-4 (rhIL-4) and TGF-β1 to simulated airway remodeling in vitro.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with OVA-induced chronic asthma, SS‑31 substantially inhibited the increase in airway responsiveness.

    In plain wordsIn mice with chronic asthma, SS‑31 reduced the rise in airway reactivity.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseAirway responsiveness
    Study

    mousen: not reported in source

    OVA-induced chronic asthma
    Outcome group
    Respiratory function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, a cuproptosis blocker, the mitochondrion-targeted antioxidant, Szeto-Schiller (SS)-31, substantially inhibited the above mentioned processes.
    3 context sentences
    Summary · context
    increased airway responsiveness, lung inflammation, area of subepithelial fibrosis and mucus hypersecretion
    Summary · context
    Repetitive OVA exposure was used to establish a mouse model of chronic asthma.
    Summary · context
    The human bronchial epithelial cell line BEAS-2B (BEAS-2B cells) was incubated with recombinant human IL-4 (rhIL-4) and TGF-β1 to simulated airway remodeling in vitro.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice with OVA-induced chronic asthma, SS‑31 substantially inhibited lung inflammation.

    In plain wordsIn mice with chronic asthma, SS‑31 reduced lung inflammation.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseLung inflammation
    Study

    mousen: not reported in source

    OVA-induced chronic asthma
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, a cuproptosis blocker, the mitochondrion-targeted antioxidant, Szeto-Schiller (SS)-31, substantially inhibited the above mentioned processes.
    3 context sentences
    Summary · context
    increased airway responsiveness, lung inflammation, area of subepithelial fibrosis and mucus hypersecretion
    Summary · context
    Repetitive OVA exposure was used to establish a mouse model of chronic asthma.
    Summary · context
    The human bronchial epithelial cell line BEAS-2B (BEAS-2B cells) was incubated with recombinant human IL-4 (rhIL-4) and TGF-β1 to simulated airway remodeling in vitro.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice with OVA-induced chronic asthma, SS‑31 substantially inhibited the increase in subepithelial fibrosis area.

    In plain wordsIn mice with chronic asthma, SS‑31 reduced scarring below the airway lining.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseSubepithelial fibrosis area
    Study

    mousen: not reported in source

    OVA-induced chronic asthma
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, a cuproptosis blocker, the mitochondrion-targeted antioxidant, Szeto-Schiller (SS)-31, substantially inhibited the above mentioned processes.
    3 context sentences
    Summary · context
    increased airway responsiveness, lung inflammation, area of subepithelial fibrosis and mucus hypersecretion
    Summary · context
    Repetitive OVA exposure was used to establish a mouse model of chronic asthma.
    Summary · context
    The human bronchial epithelial cell line BEAS-2B (BEAS-2B cells) was incubated with recombinant human IL-4 (rhIL-4) and TGF-β1 to simulated airway remodeling in vitro.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In mice with OVA-induced chronic asthma, SS‑31 substantially inhibited mucus hypersecretion.

    In plain wordsIn mice with chronic asthma, SS‑31 reduced excess mucus.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMucus hypersecretion
    Study

    mousen: not reported in source

    OVA-induced chronic asthma
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, a cuproptosis blocker, the mitochondrion-targeted antioxidant, Szeto-Schiller (SS)-31, substantially inhibited the above mentioned processes.
    3 context sentences
    Summary · context
    increased airway responsiveness, lung inflammation, area of subepithelial fibrosis and mucus hypersecretion
    Summary · context
    Repetitive OVA exposure was used to establish a mouse model of chronic asthma.
    Summary · context
    The human bronchial epithelial cell line BEAS-2B (BEAS-2B cells) was incubated with recombinant human IL-4 (rhIL-4) and TGF-β1 to simulated airway remodeling in vitro.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice with OVA-induced chronic asthma, SS‑31 substantially inhibited the rise in epithelial-mesenchymal transition protein expression (MMP-2, MMP-9, N-cadherin, vimentin, α-SMA).

    In plain wordsIn mice with chronic asthma, SS‑31 reduced proteins linked to airway tissue remodeling.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseEMT-related protein expression
    Study

    mousen: not reported in source

    OVA-induced chronic asthma
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, a cuproptosis blocker, the mitochondrion-targeted antioxidant, Szeto-Schiller (SS)-31, substantially inhibited the above mentioned processes.
    3 context sentences
    Summary · context
    expression of epithelial-mesenchymal transition (EMT)-related proteins (MMP-2, MMP-9, N-cadherin, vimentin and α-SMA)
    Summary · context
    Repetitive OVA exposure was used to establish a mouse model of chronic asthma.
    Summary · context
    The human bronchial epithelial cell line BEAS-2B (BEAS-2B cells) was incubated with recombinant human IL-4 (rhIL-4) and TGF-β1 to simulated airway remodeling in vitro.
  7. 07LabIn vitro (cells)Mechanism

    In BEAS-2B cells exposed to rhIL-4 and TGF-β1, SS‑31 at 10 ng/mL attenuated cuproptosis.

    In plain wordsIn human airway cells, SS‑31 reduced a copper-linked cell death process triggered by IL-4 and TGF-β1.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCuproptosis in BEAS-2B cells
    Study

    humann: not reported in source

    BEAS-2B bronchial epithelial cells with rhIL-4 and TGF-β1
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    10 ng/mLAs given in this study (human).

    Source sentences

    Summary
    addition of SS-31 (10 ng/mL) 30 min before rhIL-4 and TGFβ1 treatment attenuated cuproptosis
    2 context sentences
    Summary · context
    Repetitive OVA exposure was used to establish a mouse model of chronic asthma.
    Summary · context
    The human bronchial epithelial cell line BEAS-2B (BEAS-2B cells) was incubated with recombinant human IL-4 (rhIL-4) and TGF-β1 to simulated airway remodeling in vitro.

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.

PepBank is a research reference. Talk to a doctor before you use any peptide.