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Study · Animal study (in vivo) · mouse · 2013

6 results

Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing.

Evans MA, Smart N, Dubé KN, Bollini S, Clark JE, Evans HG, Taams LS, Richardson R, Lévesque M, Martin P, Mills K, Riegler J, Price AN, Lythgoe MF, Riley PR

Nature communications1 Jan 2013Cited by 67 (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 study6

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice after cardiac injury, Tβ4-sulfoxide promoted wound healing.

    In plain wordsIn mice with heart injury, Tβ4-sulfoxide helped the wound heal.

    Outcome
    IncreaseCardiac wound healing after injury
    Study

    mousen: not reported in source

    mouse cardiac injury
    Outcome group
    Wound healing · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    This function is conserved in the mouse and observed after cardiac injury, where it promotes wound healing and reduced scarring.
    1 context sentence
    Title · context
    Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice after cardiac injury, Tβ4-sulfoxide reduced scarring.

    In plain wordsIn mice with heart injury, Tβ4-sulfoxide led to less scarring.

    Outcome
    DecreaseCardiac scarring after injury
    Study

    mousen: not reported in source

    mouse cardiac injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    This function is conserved in the mouse and observed after cardiac injury, where it promotes wound healing and reduced scarring.
  3. 03LabIn vitro (cells)Mechanism

    In human T-cell/CD14+ monocyte co-cultures, Tβ4-sulfoxide inhibited interferon-γ.

    In plain wordsIn lab tests with human immune cells, Tβ4-sulfoxide lowered interferon-γ.

    Outcome
    DecreaseInterferon-γ
    Study

    humann: not reported in source

    human T-cell/CD14+ monocyte co-cultures
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In human T-cell/CD14+ monocyte co-cultures, thymosin β4-sulfoxide inhibits interferon-γ, and increases monocyte dispersal and cell death, likely by stimulating superoxide production.
  4. 04LabIn vitro (cells)Mechanism

    In human T-cell/CD14+ monocyte co-cultures, Tβ4-sulfoxide increased monocyte dispersal.

    In plain wordsIn lab tests with human immune cells, Tβ4-sulfoxide made monocytes spread out more.

    Outcome
    IncreaseMonocyte dispersal
    Study

    humann: not reported in source

    human T-cell/CD14+ monocyte co-cultures
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In human T-cell/CD14+ monocyte co-cultures, thymosin β4-sulfoxide inhibits interferon-γ, and increases monocyte dispersal and cell death, likely by stimulating superoxide production.
  5. 05LabIn vitro (cells)Mechanism

    In human T-cell/CD14+ monocyte co-cultures, Tβ4-sulfoxide increased monocyte cell death, likely by stimulating superoxide production.

    In plain wordsIn lab tests with human immune cells, Tβ4-sulfoxide increased monocyte death.

    Outcome
    IncreaseMonocyte cell death
    Study

    humann: not reported in source

    human T-cell/CD14+ monocyte co-cultures
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In human T-cell/CD14+ monocyte co-cultures, thymosin β4-sulfoxide inhibits interferon-γ, and increases monocyte dispersal and cell death, likely by stimulating superoxide production.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 06AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In wounded zebrafish, Tβ4-sulfoxide lay downstream of hydrogen peroxide and triggered depletion of inflammatory macrophages at the injury site.

    In plain wordsIn wounded zebrafish, the fish's own Tβ4-sulfoxide was linked to fewer inflammatory immune cells at the injury site.

    Outcome
    DecreaseDepletion of inflammatory macrophages at injury site
    Study

    zebrafishn: not reported in source

    wounded zebrafish
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    Here we reveal that thymosin β4-sulfoxide lies downstream of hydrogen peroxide in the wounded fish and triggers depletion of inflammatory macrophages at the injury site.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

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

    13 Oct 2026, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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