Cardiovascular disease (CVD) is a significant public health issue due to its high prevalence and considerable contribution to the global disease burden. Recent studies suggest that genetic factors, including noncoding RNAs, have an important role in the progression of CVD. Noncoding RNA plays a critical role in genetic programming and gene regulation during development. Ferroptosis is a form of iron-dependent regulated cell death (RCD), which is mainly caused by increased lipid hydroperoxide and redox imbalance. Ferroptosis is essentially different from other forms of RCD in morphology and mechanism, such as apoptosis, autophagic cell death, pyroptosis, and necroptosis. Much evidence suggested ferroptosis is involved in the development of various CVDs, especially in cardiac ischemia/reperfusion injury, heart failure, and aortic dissection. Here, we review the latest findings based on noncoding RNA regulation of ferroptosis and its involvement in the pathogenesis of CVD and related treatments, aimed at providing insights into the impact of noncoding RNA regulation of ferroptosis for CVD.
Accumulating evidence has proved that non-coding RNAs (ncRNAs) play a critical role in the genetic programming and gene regulation of cardiovascular diseases (CVDs). Cardiovascular disease morbidity and mortality are rising and have become a primary public health issue that requires immediate resolution through effective intervention. Numerous studies have revealed that new types of cell death, such as pyroptosis, necroptosis, and ferroptosis, play critical cellular roles in CVD progression. It is worth noting that ncRNAs are critical novel regulators of cardiovascular risk factors and cell functions by mediating pyroptosis, necroptosis, and ferroptosis. Thus, ncRNAs can be regarded as promising therapeutic targets for treating and diagnosing cardiovascular diseases. Recently, there has been a surge of interest in the mediation of ncRNAs on three types of cell death in regulating tissue homeostasis and pathophysiological conditions in CVDs. Although our understanding of ncRNAs remains in its infancy, the studies reviewed here may provide important new insights into how ncRNAs interact with CVDs. This review summarizes what is known about the functions of ncRNAs in modulating cell death-associated CVDs and their role in CVDs, as well as their current limitations and future prospects.
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