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Study · In vitro (cells) · 2022

3 results

Biomass-related PM2.5 induces mitochondrial fragmentation and dysfunction in human airway epithelial cells.

Gao M, Liang C, Hong W, Yu X, Zhou Y, Sun R, Li H, Huang H, Gan X, Yuan Z, Zhang J, Chen J and 5 more

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Mo Q, Wang L, Lin B, Li B, Ran P

Environmental pollution (Barking, Essex : 1987)8 Nov 2021Cited by 55 (Europe PMC)

PMID34763019 (opens in a new tab)DOI10.1016/j.envpol.2021.118464 (opens in a new tab)PepBankPUB-34763019
Publisher pagePubMedAsk about this study
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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 study3

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In 16HBE airway epithelial cells exposed to biomass PM2.5, SS‑31 eliminated mitochondrial ROS.

    In plain wordsIn lab-grown human airway cells exposed to biomass smoke particles, SS‑31 removed mitochondrial reactive oxygen species.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMitochondrial ROS
    Study

    humann: not reported in source

    16HBE human airway epithelial cells exposed to biomass-related PM2.5
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mitochondria targeted peptide SS-31 eliminated mitochondrial ROS and alleviated the ATP deficiency and proinflammatory cytokines release.
    1 context sentence
    Title · context
    Biomass-related PM2.5 induces mitochondrial fragmentation and dysfunction in human airway epithelial cells.
  2. 02LabIn vitro (cells)Efficacy outcome

    In 16HBE airway epithelial cells exposed to biomass PM2.5, SS‑31 alleviated the ATP deficiency.

    In plain wordsIn lab-grown human airway cells exposed to biomass smoke particles, SS‑31 eased the drop in cell energy (ATP).

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseATP deficiency
    Study

    humann: not reported in source

    16HBE human airway epithelial cells exposed to biomass-related PM2.5
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mitochondria targeted peptide SS-31 eliminated mitochondrial ROS and alleviated the ATP deficiency and proinflammatory cytokines release.
    1 context sentence
    Title · context
    Biomass-related PM2.5 induces mitochondrial fragmentation and dysfunction in human airway epithelial cells.
  3. 03LabIn vitro (cells)Efficacy outcome

    In 16HBE airway epithelial cells exposed to biomass PM2.5, SS‑31 alleviated proinflammatory cytokine release.

    In plain wordsIn lab-grown human airway cells exposed to biomass smoke particles, SS‑31 reduced release of inflammatory signals.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseProinflammatory cytokine release
    Study

    humann: not reported in source

    16HBE human airway epithelial cells exposed to biomass-related PM2.5
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mitochondria targeted peptide SS-31 eliminated mitochondrial ROS and alleviated the ATP deficiency and proinflammatory cytokines release.
    1 context sentence
    Title · context
    Biomass-related PM2.5 induces mitochondrial fragmentation and dysfunction in human airway epithelial cells.

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.

Publication types

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