Back to Search
Start Over
The association between ferroptosis and autophagy in cardiovascular diseases.
- Source :
-
Cell Biochemistry & Function . Mar2024, Vol. 42 Issue 2, p1-19. 19p. - Publication Year :
- 2024
-
Abstract
- Autophagy is a process in which cells degrade intracellular substances and play a variety of roles in cells, such as maintaining intracellular homeostasis, preventing cell overgrowth, and removing pathogens. It is highly conserved during the evolution of eukaryotic cells. So far, the study of autophagy is still a hot topic in the field of cytology. Ferroptosis is an iron‐dependent form of cell death, accompanied by the accumulation of reactive oxygen species and lipid peroxides. With the deepening of research, it has been found that ferroptosis, like autophagy, is involved in the occurrence and development of cardiovascular diseases. The relationship between autophagy and ferroptosis is complex, and the association between the two in cardiovascular disease remains to be clarified. This article reviews the mechanism of autophagy and ferroptosis and their correlation, and discusses the relationship between them in cardiovascular diseases, which is expected to provide new and important treatment strategies for cardiovascular diseases. Significance statement: Autophagy and ferroptosis are hot topics in the field of cell biochemistry, both of which are closely related to the occurrence and development of cardiovascular diseases. As the molecular mechanisms of autophagy and ferroptosis become more clear in cells, the two seem to intersect in some places, especially in related studies of cardiovascular diseases. If the interaction between autophagy and ferroptosis can be clarified, it will provide novel therapeutic strategies for alleviating related diseases. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 02636484
- Volume :
- 42
- Issue :
- 2
- Database :
- Academic Search Index
- Journal :
- Cell Biochemistry & Function
- Publication Type :
- Academic Journal
- Accession number :
- 176274660
- Full Text :
- https://doi.org/10.1002/cbf.3985