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Study · Measured the body's own peptide · 2021

2 results

Cardiomyocytes stimulate angiogenesis after ischemic injury in a ZEB2-dependent manner.

Gladka MM, Kohela A, Molenaar B, Versteeg D, Kooijman L, Monshouwer-Kloots J, Kremer V, Vos HR, Huibers MMH, Haigh JJ, Huylebroeck D, Boon RA, Giacca M, van Rooij E

Nature communications4 Jan 2021Cited by 91 (Europe PMC)

PMID33398012 (opens in a new tab)PMCIDPMC7782784 (opens in a new tab)DOI10.1038/s41467-020-20361-3 (opens in a new tab)PepBankPUB-33398012
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Summary

The disruption in blood supply due to myocardial infarction is a critical determinant for infarct size and subsequent deterioration in function. The identification of factors that enhance cardiac repair by the restoration of the vascular network is, therefore, of great significance. Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. Single-cell sequencing indicates ZEB2 to be enriched in injured cardiomyocytes. Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infarct healing post-myocardial infarction (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and cardiac function. We identified Thymosin β4 (TMSB4) and Prothymosin α (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models. Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA, which enhances angiogenesis and prevents cardiac dysfunction. These findings reveal ZEB2 as a beneficial factor during ischemic injury, which may hold promise for the identification of new therapies.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

No result from this study comes from a test of the peptide.

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. 01AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In the infarcted heart, therapeutic delivery of ZEB2 to cardiomyocytes induced the expression of TMSB4 and PTMA.

    In plain wordsIn infarcted hearts, delivering ZEB2 to heart muscle cells raised the body's own thymosin beta‑4 and prothymosin alpha.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseTMSB4 expression after ZEB2 delivery in the infarcted heart
    Study

    n: not reported in source

    infarcted heart with ZEB2 delivery to cardiomyocytes
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA
    1 context sentence
    Summary · context
    Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia.

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

Studies that did not test the peptide alone1

In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

  1. 02LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    Thymosin b4 and prothymosin a were identified together as paracrine factors from cardiomyocytes that stimulated angiogenesis by enhancing endothelial cell migration.

    In plain wordsIn cells, thymosin beta‑4 and prothymosin alpha released together by heart muscle cells helped blood vessel growth.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseEndothelial cell migration and angiogenesis by TMSB4 and PTMA released from cardiomyocytes
    Study

    n: not reported in source

    cardiomyocytes and endothelial cells
    Outcome group
    Angiogenesis · Cardiovascular

    Source sentences

    Summary
    We identified Thymosin β4 (TMSB4) and Prothymosin α (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models.
    1 context sentence
    Summary · context
    Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia.

    In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

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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