# Impact of follistatin-like 1 on cardiac repair processes following myocardial infarction

## TL;DR

FSTL1 is a key player in heart repair after a heart attack, influencing processes like inflammation, fibrosis, and blood vessel growth.

## Contribution

This paper provides a comprehensive review and integrated framework of FSTL1's multifaceted roles in post-infarction cardiac repair.

## Key findings

- FSTL1 promotes cardiomyocyte survival and proliferation while reducing apoptosis.
- FSTL1 modulates inflammation resolution and extracellular matrix remodeling after myocardial infarction.
- FSTL1 influences angiogenesis and neovascularization through interactions with skeletal muscle and blood circulation.

## 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.

Diagram summarizing the multifaceted roles of FSTL1 after myocardial infarction. A central panel shows a person holding the chest labeled “Myocardial infarction,” with arrows pointing to four surrounding quadrants. Top left: “Promote cardiomyocyte survival,” with decreased apoptosis and increased cell proliferation. Top right: “Anti-inflammatory response,” showing reduced inflammation. Bottom left: “Promote cardiac fibrosis,” highlighting increased pro-fibrotic response, fibroblast activation, and collagen deposition. Bottom right: “Angiogenesis/Neovascularization,” showing FSTL1 released from skeletal muscle into blood circulation and promoting vessel growth.