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Study · Measured the body's own peptide · 2023

4 results

Thymosin β4 preserves vascular smooth muscle phenotype in atherosclerosis via regulation of low density lipoprotein related protein 1 (LRP1).

Munshaw S, Redpath AN, Pike BT, Smart N

International immunopharmacology20 Jan 2023Cited by 8 (Europe PMC)

PMID37724952 (opens in a new tab)PMCIDPMC10666903 (opens in a new tab)DOI10.1016/j.intimp.2023.109702 (opens in a new tab)PepBankPUB-37724952
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Summary

Atherosclerosis is a progressive, degenerative vascular disease and a leading cause of morbidity and mortality. In response to endothelial damage, platelet derived growth factor (PDGF)-BB induced phenotypic modulation of medial smooth muscle cells (VSMCs) promotes atherosclerotic lesion formation and destabilisation of the vessel wall. VSMC sensitivity to PDGF-BB is determined by endocytosis of Low density lipoprotein receptor related protein 1 (LRP1)-PDGFR β complexes to balance receptor recycling with lysosomal degradation. Consequently, LRP1 is implicated in various arterial diseases. Having identified Tβ4 as a regulator of LRP1-mediated endocytosis to protect against aortic aneurysm, we sought to determine whether Tβ4 may additionally function to protect against atherosclerosis, by regulating LRP1-mediated growth factor signalling. By single cell transcriptomic analysis, Tmsb4x, encoding Tβ4, strongly correlated with contractile gene expression and was significantly down-regulated in cells that adopted a modulated phenotype in atherosclerosis. We assessed susceptibility to atherosclerosis of global Tβ4 knockout mice using the ApoE-/- hypercholesterolaemia model. Inflammation, elastin integrity, VSMC phenotype and signalling were analysed in the aortic root and descending aorta. Tβ4KO; ApoE-/- mice develop larger atherosclerotic plaques than control mice, with medial layer degeneration characterised by accelerated VSMC phenotypic modulation. Defects in Tβ4KO; ApoE-/- mice phenocopied those in VSMC-specific LRP1 nulls and, moreover, were underpinned by hyperactivated LRP1-PDGFRβ signalling. We identify an atheroprotective role for endogenous Tβ4 in maintaining differentiated VSMC phenotype via LRP1-mediated PDGFRβ signalling.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

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 levelOther designOther

    In single-cell transcriptomic data from atherosclerosis, Tmsb4x (Tβ4) expression correlated with contractile gene expression and was down-regulated in cells with a modulated phenotype.

    In plain wordsIn single-cell data from atherosclerosis, the body's own Tβ4 gene was lower in smooth muscle cells that had changed their state.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseTmsb4x expression in modulated smooth muscle cells
    Study

    n: not reported in source

    Outcome group
    Cardiovascular events · Cardiovascular

    Source sentences

    Summary
    By single cell transcriptomic analysis, Tmsb4x, encoding Tβ4, strongly correlated with contractile gene expression and was significantly down-regulated in cells that adopted a modulated phenotype in atherosclerosis.

    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 alone3

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. 02AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome

    In ApoE-/- mice, loss of Tβ4 (knockout) led to larger atherosclerotic plaques than in control mice.

    In plain wordsIn mice prone to atherosclerosis, removing the Tβ4 gene gave larger artery plaques than in control mice.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseAtherosclerotic plaque size
    Study

    mousen: not reported in source

    ApoE-/- hypercholesterolaemia, global Tβ4 knockout
    Comparator
    Control mice
    Outcome group
    Cardiovascular events · Cardiovascular

    Source sentences

    Summary
    Tβ4KO; ApoE-/- mice develop larger atherosclerotic plaques than control mice, with medial layer degeneration characterised by accelerated VSMC phenotypic modulation.
    1 context sentence
    Summary · context
    We assessed susceptibility to atherosclerosis of global Tβ4 knockout mice using the ApoE-/- hypercholesterolaemia model.

    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).

  2. 03AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome

    In ApoE-/- mice, loss of Tβ4 caused medial layer degeneration with accelerated phenotypic modulation of vascular smooth muscle cells.

    In plain wordsIn mice prone to atherosclerosis, removing the Tβ4 gene damaged the artery wall layer and sped up smooth muscle cell change.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseMedial layer degeneration and VSMC phenotypic modulation
    Study

    mousen: not reported in source

    ApoE-/- hypercholesterolaemia, global Tβ4 knockout
    Comparator
    Control mice
    Outcome group
    Cardiovascular events · Cardiovascular

    Source sentences

    Summary
    Tβ4KO; ApoE-/- mice develop larger atherosclerotic plaques than control mice, with medial layer degeneration characterised by accelerated VSMC phenotypic modulation.
    1 context sentence
    Summary · context
    We assessed susceptibility to atherosclerosis of global Tβ4 knockout mice using the ApoE-/- hypercholesterolaemia model.

    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).

  3. 04AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Mechanism

    In ApoE-/- mice, loss of Tβ4 produced defects that phenocopied VSMC-specific LRP1 nulls and were underpinned by hyperactivated LRP1-PDGFRβ signalling.

    In plain wordsIn mice prone to atherosclerosis, removing the Tβ4 gene overactivated a growth signal in artery wall cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseLRP1-PDGFRβ signalling
    Study

    mousen: not reported in source

    ApoE-/- hypercholesterolaemia, global Tβ4 knockout
    Comparator
    Control mice
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Defects in Tβ4KO; ApoE-/- mice phenocopied those in VSMC-specific LRP1 nulls and, moreover, were underpinned by hyperactivated LRP1-PDGFRβ signalling.
    1 context sentence
    Summary · context
    We assessed susceptibility to atherosclerosis of global Tβ4 knockout mice using the ApoE-/- hypercholesterolaemia model.

    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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