PiRNA in Cardiovascular Disease: Focus on Cardiac Remodeling and Cardiac Protection

Cardiovascular diseases (CVDs) are common causes of death, which take about 18.6 million lives worldwide every year. Currently, exploring strategies that delay ventricular remodeling, reduce cardiomyocyte death, and promote cardiomyocyte regeneration has been the hotspot and difficulty of the ischem...

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Veröffentlicht in:Journal of cardiovascular translational research 2023-08, Vol.16 (4), p.768-777
Hauptverfasser: Zhang, Kaiyu, Li, Yafei, Huang, Ying, Sun, Kangyun
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Sprache:eng
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Zusammenfassung:Cardiovascular diseases (CVDs) are common causes of death, which take about 18.6 million lives worldwide every year. Currently, exploring strategies that delay ventricular remodeling, reduce cardiomyocyte death, and promote cardiomyocyte regeneration has been the hotspot and difficulty of the ischemic heart disease (IHD) research field. Previous studies indicate that piwi-interacting RNA (piRNA) plays a vital role in the occurrence and development of cardiac remodeling and may offer novel therapeutic strategies for cardiac repair. The best-known biological function of piRNA is to silence transposons in cells. In the cardiovascular system, piRNA is known to participate in cardiac progenitor cell proliferation, AKT pathway regulation, and cardiac remodeling and decompensation. In this review, we systematically discuss the research progress on piRNA in CVDs, especially the mechanism of cardiac remodeling and the potential functions in cardiac protection, which provides new insights for the progress and treatment of cardiovascular diseases. Graphical abstract Piwi-interacting RNA (piRNA) is one of the noncoding RNAs, with the best -known biological function to silence transposons in cells. Now piRNA is found to participate in cardiac progenitor cell proliferation, AKT pathway regulation, cardiac remodeling and decompensation, which implies the potential of piRNA in the diagnosis and treatment of cardiovascular diseases. Over expression of piRNA could promote cardiac apoptosis and cardiac hypertrophy, thus targeted therapy which inhibits expression of associated piRNA may reduce cardiac remodeling and reduce inflammation caused by necrotic cardiomyocytes. PiRNA is also speculated to participate in the proliferation of cardiac progenitor cells, implying the potential to induce cardiac regeneration th erapy, which provides new insights for treatment of cardiovascular diseases. At present, the treatment strategy of cardiac remodeling emphasizes the control of risk factors, prevention of disease progression and individualized treatment. With further studies in mechanism of piRNA, potential therapies above may come true and more therapies in cardiovascular diseases may be found.
ISSN:1937-5387
1937-5395
DOI:10.1007/s12265-023-10353-1