ReviewFrontiers in cell and developmental biology2025
Impact of follistatin-like 1 on cardiac repair processes following myocardial infarction.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Exercise Intensity and Circulating Exerkine Responses: A Narrative Review of Selected Molecules.Biomolecules · 2026Review
- Systemic responses to intravenous rAAV administration in boys with Duchenne muscular dystrophy.Frontiers in molecular medicine · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Follistatin-like 1 (FSTL1) is an emerging multifunctional glycoprotein that plays a central role in cardiac repair following myocardial infarction (MI). While previous studies have explored its involvement in modulating inflammation, angiogenesis, and fibrosis, a cohesive mechanistic understanding remains incomplete. In this review, we provide a comprehensive synthesis of current findings and propose an integrated framework in which FSTL1 orchestrates post-infarction healing through multiple signaling cascades, including BMP/SMAD, PI3K/AKT, MAPK, and TGF-β pathways. We highlight its dual actions in both cardiomyocytes and cardiac fibroblasts, as well as its context-dependent interactions with mechanical cues and the immune microenvironment. Recent evidence suggests that FSTL1 may function as a key regulatory hub, coordinating sequential events such as inflammation resolution, extracellular matrix remodeling, and functional recovery. Together, these insights underscore the therapeutic promise of FSTL1 as a molecular target for enhancing cardiac repair and restoring myocardial integrity after infarction.
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