Key result
Endothelial-to-mesenchymal transition contributes to the development of various cardiovascular diseases, including atherosclerosis, valve diseases, fibrosis, and pulmonary arterial hypertension.
Why the study?
Endothelial-to-mesenchymal transition contributes to cardiovascular disease development, and a deeper understanding of its cellular and molecular mechanisms is urgently needed to provide insights into reversing this condition.
This review highlights the cellular and molecular mechanisms of endothelial-to-mesenchymal transition in cardiovascular diseases, providing insights for potential therapeutic targets.
Endothelial-to-mesenchymal transition (EndoMT) is the process of endothelial cells progressively losing endothelial-specific markers and gaining mesenchymal phenotypes. In the normal physiological condition, EndoMT plays a fundamental role in forming the cardiac valves of the developing heart. However, EndoMT contributes to the development of various cardiovascular diseases (CVD), such as atherosclerosis, valve diseases, fibrosis, and pulmonary arterial hypertension (PAH). Therefore, a deeper understanding of the cellular and molecular mechanisms underlying EndoMT in CVD should provide urgently needed insights into reversing this condition. This review summarizes a 30-year span of relevant literature, delineating the EndoMT process in particular, key signaling pathways, and the underlying regulatory networks involved in CVD.
No takes yet. Share an insight, caveat, or question.
Peng et al. (2022) conducted a review in Cardiovascular disease. Endothelial-to-mesenchymal transition (EndoMT) was evaluated. Endothelial-to-mesenchymal transition contributes to the development of various cardiovascular diseases, including atherosclerosis, valve diseases, fibrosis, and pulmonary arterial hypertension.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: