A promising field: regulating imbalance of EndMT in cardiovascular diseases

Cell Cycle. 2021 Aug;20(15):1477-1486. doi: 10.1080/15384101.2021.1951939. Epub 2021 Jul 16.

Abstract

Endothelial-mesenchymal transition (EndMT) is widely involved in the occurrence and development of cardiovascular diseases. Although there is no direct evidence, it is very promising as an effective target for the treatment of these diseases. Endothelial cells need to respond to the complex cardiovascular environment through EndMT, but sustained stimuli will cause the imbalance of EndMT. Blocking the signal transduction promoting EndMT is an effective method to control the imbalance of EndMT. In particular, we also discussed the potential role of endothelial cell apoptosis and autophagy in regulating the imbalance of EndMT. In addition, promoting mesenchymal-endothelial transformation (MEndT) is also a method to control the imbalance of EndMT. However, targeting EndMT to treat cardiovascular disease still faces many challenges. By reviewing the research progress of EndMT, we have put forward some insights and translated them into challenges and opportunities for new treatment strategies for cardiovascular diseases.

Keywords: Cardiovascular diseases; apoptosis; autophagy; endmt; mendt.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Autophagy
  • Cardiovascular Agents / therapeutic use
  • Cardiovascular Diseases / drug therapy
  • Cardiovascular Diseases / metabolism
  • Cardiovascular Diseases / pathology*
  • Cell Plasticity
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Endothelial Cells / pathology*
  • Epithelial-Mesenchymal Transition* / drug effects
  • Humans
  • Phenotype
  • Signal Transduction

Substances

  • Cardiovascular Agents

Grants and funding

This work was supported by the National Natural Science Foundation of China [670429]; National Natural Science Foundation of China [81470435]; National Natural Science Foundation of China [9183910381].