Key result
Myeloid-derived GARP and LRG1 regulate local TGF-β signaling to drive cardiac repair after MI.
Why the study?
Although the opposing inflammatory and reparative functions of TGF-β in post-infarct myocardial remodeling have traditionally been attributed to signaling timing, increasing evidence suggests that local regulatory mechanisms within the infarct microenvironment critically shape its pathophysiological effects.
This review highlights the roles of myeloid-derived modulators GARP and LRG1 in regulating local TGF-beta signaling during post-infarct myocardial remodeling, identifying them as potential therapeutic targets.
Answers are grounded in this paper and cite their sources.
Myeloid modulators may refine TGF-β targeting in post-MI remodeling; leaves open context-specific therapies pending validation.
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.
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Fujio et al. (2026) conducted a review in Post-infarct myocardial remodeling. Myeloid-derived modulators of TGF-β (GARP and LRG1) was evaluated on Transition from inflammatory injury to reparative remodeling post-MI. Myeloid-derived modulators GARP and LRG1 shape local TGF-β signaling niches to orchestrate the transition from inflammatory injury to reparative remodeling after myocardial infarction.
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