Go to
JCI Insight
Abstract
In humans, the biological limitations to cardiac regenerative growth create both a clinical imperative — to offset cell death in acute ischemic injury and chronic heart failure — and a clinical opportunity; that is, for using cells, genes, and proteins to rescue cardiac muscle cell number or in other ways promote more efficacious cardiac repair. Recent experimental studies and early-phase clinical trials lend credence to the visionary goal of enhancing cardiac repair as an achievable therapeutic target.
Authors
Stefanie Dimmeler, Andreas M. Zeiher, Michael D. Schneider
Figure 2
Options:
View larger image
(or click on image)
Download as PowerPoint
Mechanisms of action. Progenitor cells may improve functional recovery of infarcted or failing myocardium by various potential mechanisms, including direct or indirect improvement of neovascularization. Paracrine factors released by progenitor cells may inhibit cardiac apoptosis, affect remodeling, or enhance endogenous repair (e.g., by tissue-resident progenitor cells). Differentiation into cardiomyocytes may contribute to cardiac regeneration. The extent to which these different mechanisms are active may critically depend on the cell type and setting, such as acute or chronic injury.
Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)