A Narrative Review on the FSTL-1 Protein and its Current Known Impact on Cardiovascular Ischaemic Disease

Authors

DOI:

https://doi.org/10.5195/ijms.2024.2297

Keywords:

Myocardial Ischemia, Coronary Artery Disease, Follistatin-Related Proteins, Follistatin-Related Protein 1 , FSTL-1 Protein, Cardiovascular Regeneration, Myocardial Infarction, Ischaemic Heart Disease, Cardiac Stem Cells, Anti-Inflammatory Properties, Angiogenesis, Fibrosis Reduction, AKT and ERK Pathways, Therapeutic Target

Abstract

This narrative review investigates the potential therapeutic role of FSTL-1 in addressing severe cardiac issues following myocardial infarctions (MI). Despite advances in modern medicine, MI persist as a leading global cause of death, with stem cell therapy falling short of expectations since the early 2000s. In contrast, FSTL-1, an emerging bone morphogenetic protein, demonstrates promise based on successful studies. We conducted a qualitative narrative synthesis of studies published in PubMed, Scopus, and Web of Science between January 2000 and May 2022. This research explores the intricate scientific aspects of FSTL-1's contribution to myocardial regeneration, utilizing a chronological approach to trace its progression from biological pathways to broader scenarios. It examines the mechanisms regulated by FSTL-1 and its effects on cardiac tissue and cells, highlighting its potential as a therapeutic agent emphasizing its multifaceted role in cardiac regeneration. By deepening our comprehension of FSTL-1, this study significantly contributes to knowledge advancement, offering insights into its role in addressing severe cardiac issues post-MI. By consolidating current knowledge and proposing new avenues for investigation, this work offers valuable insights into FSTL-1's significance in advancing cardiovascular health and post-MI recovery.

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This diagram depicts signaling pathways involving FSTL-1 and its role in cardiomyocyte growth, apoptosis, and proliferation. The image shows multiple pathways and interactions. FSTL-1 (Follistatin-like 1) is positioned at the center and connects to two primary pathways: one leading to cardiomyocyte growth and the other to cardiomyocyte proliferation. On the left, FSTL-1 interacts with α1β2α and activates the PI3K pathway, leading to Akt activation. Akt then influences downstream targets such as p53 and eNOS, which block cardiomyocyte apoptosis via Bcl-2 and NO production. Simultaneously, the AMPK pathway inhibits TSC1/TSC2, which activates mTORC1, promoting cardiomyocyte growth. On the right, FSTL-1 interacts with BMP receptors (BmPRII) and activates the ERK 1/2 pathway, leading to fibroblast activation and cardiomyocyte proliferation. This pathway also involves Smad1/5/8 signaling, contributing to inflammatory responses and preventing heart rupture. The diagram uses various shapes, solid and dashed arrows, to represent signaling cascades and outcomes, emphasizing the role of FSTL-1 in cardiomyocyte survival and repair.

Published

2024-11-20 — Updated on 2024-12-17

How to Cite

Rodrigues Gomes, J. (2024). A Narrative Review on the FSTL-1 Protein and its Current Known Impact on Cardiovascular Ischaemic Disease. International Journal of Medical Students, 12(4), 457–464. https://doi.org/10.5195/ijms.2024.2297