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April 12, 2026International Journal of Molecular SciencesOpen Access

ML216 Alleviates Age-Related Cardiac Fibrosis by Suppressing TGF-β1 Signaling Pathway

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Why the study?

Does the small-molecule compound ML216 alleviate cardiac fibrosis in aging-associated or isoproterenol-induced models?

Population

In vitro and in vivo models of aging-associated or β-adrenoceptor agonist isoproterenol-induced cardiac…

Design

Preclinical

Authors

WLWenbin LiuFCFeng CuiXHXiaodan Huang

Discussion

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Overview

ML216 represents a potential therapeutic candidate for treating age-related and isoproterenol-induced cardiac fibrosis by targeting the TGF-β1 signaling pathway.

Key Points

  • This research investigates the effects of ML216 on age-related cardiac fibrosis and its underlying mechanisms.
  • In vitro and in vivo testing of ML216 on cardiac fibrosis
  • Assessment of TGF-β1 signaling inhibition
  • Measurement of fibrotic gene expression and cardiomyocyte apoptosis
  • ML216 significantly reduces TGF-β1 protein levels and SMAD phosphorylation
  • Decreased expression of fibrotic genes including Col1a1, Cnn2, and Acta2
  • Alleviated cardiomyocytes apoptosis linked to reduced inflammatory responses

Structured PICO

Does the small-molecule compound ML216 alleviate cardiac fibrosis in aging-associated or isoproterenol-induced models?

P
Population
In vitro and in vivo models of aging-associated or β-adrenoceptor agonist isoproterenol-induced cardiac fibrosis
I
Intervention
Small-molecule compound ML216
O
Outcome
Cardiac fibrosissurrogate

ML216 represents a potential therapeutic candidate for treating age-related and isoproterenol-induced cardiac fibrosis by targeting the TGF-β1 signaling pathway.

Cite This Study

Liu et al. (2026) studied this question.

synapsesocial.com/papers/69db37ca4fe01fead37c5df4https://doi.org/10.3390/ijms27083425
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