Skip to content

Study · Not a test of the peptide alone · 2021

6 results

Thymosin β4 protects against aortic aneurysm via endocytic regulation of growth factor signaling.

Munshaw S, Bruche S, Redpath AN, Jones A, Patel J, Dubé KN, Lee R, Hester SS, Davies R, Neal G, Handa A, Sattler M, Fischer R, Channon KM, Smart N

The Journal of clinical investigation1 May 2021Cited by 30 (Europe PMC)

PMID33784254 (opens in a new tab)PMCIDPMC8121525 (opens in a new tab)DOI10.1172/jci127884 (opens in a new tab)PepBankPUB-33784254
Download PDFPubMedAsk about this study
Jump to 6 results

Summary

Vascular stability and tone are maintained by contractile smooth muscle cells (VSMCs). However, injury-induced growth factors stimulate a contractile-synthetic phenotypic modulation which increases susceptibility to abdominal aortic aneurysm (AAA). As a regulator of embryonic VSMC differentiation, we hypothesized that Thymosin β4 (Tβ4) may function to maintain healthy vasculature throughout postnatal life. This was supported by the identification of an interaction with low density lipoprotein receptor related protein 1 (LRP1), an endocytic regulator of platelet-derived growth factor BB (PDGF-BB) signaling and VSMC proliferation. LRP1 variants have been implicated by genome-wide association studies with risk of AAA and other arterial diseases. Tβ4-null mice displayed aortic VSMC and elastin defects that phenocopy those of LRP1 mutants, and their compromised vascular integrity predisposed them to Angiotensin II-induced aneurysm formation. Aneurysmal vessels were characterized by enhanced VSMC phenotypic modulation and augmented PDGFR-β signaling. In vitro, enhanced sensitivity to PDGF-BB upon loss of Tβ4 was associated with dysregulated endocytosis, with increased recycling and reduced lysosomal targeting of LRP1-PDGFR-β. Accordingly, the exacerbated aneurysmal phenotype in Tβ4-null mice was rescued upon treatment with the PDGFR-β antagonist Imatinib. Our study identifies Tβ4 as a key regulator of LRP1 for maintaining vascular health, and provides insights into the mechanisms of growth factor-controlled VSMC phenotypic modulation underlying aortic disease progression.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

Studies that did not test the peptide alone6

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. 01AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Other

    Tβ4-null mice displayed aortic vascular smooth muscle cell and elastin defects that resemble those of LRP1 mutants.

    In plain wordsIn mice lacking Tβ4, the aorta showed smooth muscle cell and elastin defects.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseAortic smooth muscle cell and elastin defects in Tβ4-null mice
    Study

    mousen: not reported in source

    Tβ4-null mice
    Outcome group
    Cardiovascular events · Cardiovascular

    Source sentences

    Summary
    Tβ4-null mice displayed aortic VSMC and elastin defects that phenocopy those of LRP1 mutants, and their compromised vascular integrity predisposed them to Angiotensin II-induced aneurysm formation.

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

    Compromised vascular integrity in Tβ4-null mice predisposed them to Angiotensin II-induced aneurysm formation.

    In plain wordsIn mice lacking Tβ4, the aorta was more prone to aneurysm after angiotensin II.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseAngiotensin II-induced aneurysm formation in Tβ4-null mice
    Study

    mousen: not reported in source

    Tβ4-null mice
    Outcome group
    Cardiovascular events · Cardiovascular

    Source sentences

    Summary
    Tβ4-null mice displayed aortic VSMC and elastin defects that phenocopy those of LRP1 mutants, and their compromised vascular integrity predisposed them to Angiotensin II-induced aneurysm formation.

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

    Aneurysmal vessels of Tβ4-null mice showed enhanced VSMC phenotypic modulation and augmented PDGFR-β signaling.

    In plain wordsIn mice lacking Tβ4, aneurysm vessels showed stronger smooth muscle cell change and growth-factor signaling.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseVSMC phenotypic modulation and PDGFR-β signaling in aneurysmal vessels
    Study

    mousen: not reported in source

    Tβ4-null mice
    Outcome group
    Cardiovascular events · Cardiovascular

    Source sentences

    Summary
    Aneurysmal vessels were characterized by enhanced VSMC phenotypic modulation and augmented PDGFR-β signaling.
    1 context sentence
    Summary · context
    Tβ4-null mice displayed aortic VSMC and elastin defects that phenocopy those of LRP1 mutants, and their compromised vascular integrity predisposed them to Angiotensin II-induced aneurysm formation.

    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).

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

    The exacerbated aneurysmal phenotype in Tβ4-null mice was rescued by treatment with the PDGFR-β antagonist imatinib.

    In plain wordsIn mice lacking Tβ4, the drug imatinib reversed the worse aneurysm outcome.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseAneurysmal phenotype in Tβ4-null mice treated with imatinib
    Study

    mousen: not reported in source

    Tβ4-null mice
    Comparator
    Untreated Tβ4-null mice
    Outcome group
    Cardiovascular events · Cardiovascular

    Source sentences

    Summary
    Accordingly, the exacerbated aneurysmal phenotype in Tβ4-null mice was rescued upon treatment with the PDGFR-β antagonist Imatinib.
    1 context sentence
    Summary · context
    Tβ4-null mice displayed aortic VSMC and elastin defects that phenocopy those of LRP1 mutants, and their compromised vascular integrity predisposed them to Angiotensin II-induced aneurysm formation.

    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).

  5. 05LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    An interaction between Tβ4 and low density lipoprotein receptor related protein 1 (LRP1) was identified.

    In plain wordsIn lab tests, Tβ4 was found to interact with the receptor protein LRP1.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableInteraction of Tβ4 with LRP1
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    This was supported by the identification of an interaction with low density lipoprotein receptor related protein 1 (LRP1), an endocytic regulator of platelet-derived growth factor BB (PDGF-BB) signaling and VSMC proliferation.

    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).

  6. 06LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In vitro, loss of Tβ4 enhanced sensitivity to PDGF-BB and was associated with dysregulated endocytosis, with increased recycling and reduced lysosomal targeting of LRP1-PDGFR-β.

    In plain wordsIn cells, losing Tβ4 increased sensitivity to a growth factor and disturbed how a receptor complex is handled.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreasePDGF-BB sensitivity and LRP1-PDGFR-β endocytosis after Tβ4 loss
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    In vitro, enhanced sensitivity to PDGF-BB upon loss of Tβ4 was associated with dysregulated endocytosis, with increased recycling and reduced lysosomal targeting of LRP1-PDGFR-β.
    1 context sentence
    Summary · context
    Tβ4-null mice displayed aortic VSMC and elastin defects that phenocopy those of LRP1 mutants, and their compromised vascular integrity predisposed them to Angiotensin II-induced aneurysm formation.

    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.

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