The crosstalk among autophagy, apoptosis, and pyroptosis in cardiovascular disease

Abstract

In recent years, the mechanism of cell death has become a hotspot in research on the pathogenesis and treatment of cardiovascular disease (CVD). Different cell death modes, including autophagy, apoptosis, and pyroptosis, are mosaic with each other and collaboratively regulate the process of CVD. This review summarizes the interaction and crosstalk of key pathways or proteins which play a critical role in the entire process of CVD and explores the specific mechanisms. Furthermore, this paper assesses the interrelationships among these three cell deaths and reviews how they regulate the pathogenesis of CVD. By understanding how these three cell death modes go together we can learn about the pathogenesis of CVD, which will enable us to identify new targets for preventing, controlling, and treating CVD. It will not only reduce mortality but also improve the quality of life.

Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

“…Unlike other forms of cell death, apoptosis does not release cellular contents that can trigger inflammation, making it a more controlled and regulated mechanism of cell death. [39][40][41] Apoptosis has a significant impact on the development of various cardiovascular diseases. Unlike other forms of cell death, apoptosis does not release harmful contents that can cause inflammation and damage surrounding cells or tissues.…”

“…Apoptosis is a key process in the development and progression of various cardiovascular diseases. Unlike other forms of cell death, apoptosis does not release cellular contents that can trigger inflammation, making it a more controlled and regulated mechanism of cell death 39–41 . Apoptosis has a significant impact on the development of various cardiovascular diseases.…”

The ameliorating effects of mesenchymal stem cells compared to α‐tocopherol on apoptosis and autophagy in streptozotocin‐induced diabetic rats: Implication of PI3K/Akt signaling pathway and entero‐insular axis

“…it becomes impaired then ubiquitinated proteins and autophagosomes are accumulated and autophagy fails, and programmed cell death becomes, therefore, activated. 43,44 In view of our data, diabetic untreated rats showed increased oxidative stress and defective autophagy that are associated with increased apoptosis-related caspase 3. The cytoprotective effects of BM-MSCs and α-Toc on β cells involved reduced apoptosis that could be related to the antioxidant effect and the upregulated autophagy.…”

“…Whereas secondary to any deleterious events. it becomes impaired then ubiquitinated proteins and autophagosomes are accumulated and autophagy fails, and programmed cell death becomes, therefore, activated 43,44 …”

Stellettin B Induces Cell Death in Bladder Cancer Via Activating the Autophagy/DAPK2/Apoptosis Signaling Cascade

“…After that, the autophagosomes are conjugated with the lysosome to degrade the cellular components. Autophagy and apoptosis represent the two conserved intracellular processes that can regulate cell survival and death under stress conditions, and their crosstalk has also been reported [ 22 ]. For example, nonconjugated ATG5 is cleaved by calpain, and its product, ATG5tN, enters the mitochondria to promote the release of cytochrome c [ 23 ].…”