Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Cardiol. May 26, 2026; 18(5): 119321
Published online May 26, 2026. doi: 10.4330/wjc.v18.i5.119321
Published online May 26, 2026. doi: 10.4330/wjc.v18.i5.119321
Mechanistic convergence of exercise and mesenchymal stem cell-derived exosome signaling in isoproterenol-induced myocardial injury
Jacob Strouse, Stevenson Cottiere, Herbert Wertheim College of Medicine, Florida Inter national University, Miami, FL 33138, United States
Brandon Lucke-Wold, Lillian S. Wells Department of Neurosurgery, University of Florida, Gainesville, FL 32608, United States
Author contributions: Strouse J designed the concept and outline; Strouse J and Cottiere S performed the literature review and drafted the manuscript; all authors critically revised the manuscript; Lucke-Wold B approved the final version.
Conflict-of-interest statement: The authors declare no conflicts of interest.
Corresponding author: Jacob Strouse, Herbert Wertheim College of Medicine, Florida International University, 11200 SW 8th St AHC2, Miami, FL 33138, United States. jstro026@fiu.edu
Received: February 2, 2026
Revised: March 5, 2026
Accepted: April 10, 2026
Published online: May 26, 2026
Processing time: 115 Days and 9.9 Hours
Revised: March 5, 2026
Accepted: April 10, 2026
Published online: May 26, 2026
Processing time: 115 Days and 9.9 Hours
Core Tip
Core Tip: Exercise primes cardiomyocyte stress tolerance through ERK and PI3K/Akt/mTOR pathway activation, regulated autophagy, and mitochondrial preservation, while mesenchymal stem cell-derived exosomes reinforce these same survival networks via paracrine delivery of bioactive cargo. Integrating exercise conditioning with targeted, cell-free exosome-based strategies may overcome current therapeutic plateaus by enhancing biological engagement, improving myocardial resilience, and biasing post-ischemic remodeling toward adaptive recovery.