p53 contributes to cardiovascular diseases via mitochondria dysfunction: A new paradigm

Area of Science:

• Biomedical Science
• Cardiovascular Research
• Mitochondrial Biology

Background:

• Cardiovascular diseases (CVDs) are a major global health concern with unclear underlying mechanisms.
• The tumor suppressor p53, known for its role in cancer, also significantly influences cardiovascular health.
• Mitochondrial dysfunction is increasingly recognized as a critical factor in the development of CVDs.

Purpose of the Study:

• To comprehensively review the mechanisms by which p53 influences mitochondrial dysfunction in various CVDs.
• To explore the interplay between p53 abnormalities and mitochondrial dysfunction.
• To discuss the therapeutic potential of targeting p53 or mitochondria for CVD treatment.

Main Methods:

• Literature review of studies investigating p53, mitochondrial dysfunction, and cardiovascular diseases.
• Analysis of mechanisms including energy metabolism, oxidative stress, apoptosis, autophagy, and dynamics.
• Synthesis of findings on small molecule inhibitors and mitochondrial-based therapies.

Main Results:

• Abnormal p53 expression and modifications are linked to CVD occurrence and progression.
• p53 abnormalities directly correlate with and may interact with mitochondrial dysfunction.
• Targeting p53 with small molecule inhibitors shows efficacy in animal models of CVDs.

Conclusions:

• Targeting p53 or mitochondria presents a promising, pioneering therapeutic strategy for combating CVDs.
• Further research into the p53-mitochondria axis can unlock novel treatment avenues for cardiovascular conditions.
• Mitochondrial replacement therapy and targeting mitochondrial-related molecules offer advantageous therapeutic potential.