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Updated: Jun 21, 2026

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
Renal studies provide an insight into cardiac extracellular matrix remodeling during health and disease
Alexandre Hertig1, Taduri Gangadhar, Raghu Kalluri
1Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, USA.
Insights
Heart and kidney injuries trigger fibrotic remodeling through cell transitions like EMT and EndMT. Future therapies may target shared mechanisms for tissue repair and improved organ function.
Area of Science:
- Cardiovascular and Renal Pathophysiology
- Tissue Remodeling and Fibrogenesis
Background:
- Myocardial infarction and kidney injury initiate inflammatory processes leading to fibrotic remodeling and organ dysfunction.
- Abnormal extracellular matrix deposition is a hallmark of chronic kidney disease and cardiac remodeling.
Purpose of the Study:
- To explore the shared mechanisms of injury and fibrogenesis in the heart and kidney.
- To highlight recent advances in understanding matrix remodeling and potential therapeutic targets.
Main Methods:
- Review of recent literature on cardiac and renal injury.
- Analysis of cellular plasticity, including epithelial-to-mesenchymal transition (EMT) and endothelial-to-mesenchymal transition (EndMT).
- Investigation of the role of the fibrinolytic system and stem cell integration in tissue repair.
Main Results:
- Epithelial and endothelial cells actively contribute to fibrogenesis via EMT and EndMT.
- Fibrinolytic system components exhibit novel interactions with cellular receptors and integrins.
- Stem cell integration is a newly recognized factor in tissue repair following injury.
Conclusions:
- The heart and kidney share common injury mechanisms contributing to fibrotic remodeling.
- Understanding these shared pathways, including EMT, EndMT, and stem cell roles, offers potential for novel, common therapeutic strategies.
- Targeting matrix remodeling processes presents a promising avenue for treating both cardiac and renal diseases.
Abstract:
The remodeling of a heart ventricle after myocardial infarction involves numerous inflammatory mediators that may trigger a long-lasting and a highly fibrogenic process. Likewise, in the kidney, acute and chronic injuries may lead to abnormal extracellular matrix deposition and eventually lead to the loss of renal function. Major breakthroughs have emerged during the last ten years with respect to the pathophysiology of matrix remodeling. Epithelial and endothelial cells are plastic, and able to engage in epithelial (or endothelial)-to-mesenchymal transition (EMT or EndMT), thus actively contributing to the fibrogenesis. Members of the fibrinolytic system were demonstrated to possess unsuspected properties and interact with receptors and integrins on endothelial and epithelial cells. Finally, a notion that stem cells could integrate into damaged tissue has recently emerged, which likely contributes to the tissue repair. In many aspects, the kidney and the heart share many common injury mechanisms. We envision that some of them will be accessible as common therapeutic targets in the future.
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