ABSTRACT
As a result of ongoing breakthroughs in cancer therapy, cancer patients' survival rates have grown considerably. However, cardiotoxicity has emerged as the most dangerous toxic side effect of cancer treatment, negatively impacting cancer patients' prognosis. In recent years, the link between non-coding RNAs (ncRNAs) and cancer therapy-induced cardiotoxicity has received much attention and investigation. NcRNAs are non-protein-coding RNAs that impact gene expression post-transcriptionally. They include microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). In several cancer treatments, such as chemotherapy, radiotherapy, and targeted therapy-induced cardiotoxicity, ncRNAs play a significant role in the onset and progression of cardiotoxicity. This review focuses on the mechanisms of ncRNAs in cancer therapy-induced cardiotoxicity, including apoptosis, mitochondrial damage, oxidative stress, DNA damage, inflammation, autophagy, aging, calcium homeostasis, vascular homeostasis, and fibrosis. In addition, this review explores potential ncRNAs-based biomarkers and therapeutic strategies, which may help to convert ncRNAs research into clinical practice in the future for early detection and improvement of cancer therapy-induced cardiotoxicity.
ABSTRACT
The nod-like receptor family pyrin domain containing 3 (NLRP3) is currently the most widely studied inflammasome and has become a hot topic of recent research. As a macromolecular complex, the NLRP3 inflammasome is activated to produce downstream factors, including caspase-1, IL-1ß, and IL-18, which then promote local inflammatory responses and induce pyroptosis, leading to unfavorable effects. A growing number of studies have examined the relationship between the NLRP3 inflammasome and cardiovascular diseases (CVDs). However, some studies have shown that the NLRP3 inflammasome is not involved in the occurrence of certain diseases. Therefore, identifying the mechanism of action of the NLRP3 inflammasome and its potential involvement in the pathological process of disease progression is of utmost importance. This review discusses the mechanisms of NLRP3 inflammasome activation and the relationship between the inflammasome and CVDs, including coronary atherosclerosis, myocardial ischemia/reperfusion, cardiomyopathies, and arrhythmia, as well as CVD-related treatments.