Myeloid-derived modulators shape the pathophysiological roles of TGF-β in post-infarct myocardial remodeling.

Authors

Yasushi Fujio, Shota Tanaka, Keisuke Shirakura, Yoshiaki Okada, Masanori Obana

Published in

American journal of physiology. Heart and circulatory physiology. Nov 02, 2026. Epub Nov 02, 2026.

Abstract

Transforming growth factor-β (TGF-β) plays diverse roles in post-infarct myocardial remodeling, ranging from inflammatory injury to tissue repair. Although these apparently opposing functions have traditionally been attributed to the timing of TGF-β signaling, increasing evidence suggests that local regulatory mechanisms within the infarct microenvironment critically shape its pathophysiological effects. In this review, we propose that myeloid-derived modulators define the context-dependent pathophysiological roles of TGF-β after myocardial infarction. We focus on two mechanistically distinct regulators: glycoprotein A repetitions predominant (GARP), a membrane-bound activator of latent TGF-β that promotes localized inflammatory signaling, and leucine-rich α2-glycoprotein-1 (LRG1), a secreted modulator that promotes angiogenesis and tissue repair. We discuss the emerging importance of these mechanistically distinct regulators in shaping local TGF-β signaling niches that orchestrate the transition from inflammatory injury to reparative remodeling and highlight their potential as therapeutic targets for precision modulation of post-infarct remodeling.

PMID:
42968666
Bibliographic data and abstract were imported from PubMed on 02 Nov 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.