Cellular and Extracellular Non-coding RNAs in Cardiac Physiology and Diseases
Cellular and Extracellular Non-coding RNAs in Cardiac Physiology and Diseases
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DOI:
10.1007/s12265-022-10270-9
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发表时间:
2022-05
影响因子:
3.4
通讯作者:
Tingting Yang;Songwei Ai;P. Gokulnath;Guoping Li;Junjie Xiao
中科院分区:
文献类型:
--
作者:
Tingting Yang;Songwei Ai;P. Gokulnath;Guoping Li;Junjie Xiao
Despite considerable advances over the past 20 years, cardiovascular diseases (CVDs) have persisted as the leading global cause of illnesses and deaths. CVDs trigger adverse cardiac remodeling, manifested by hypertrophy, inflammation, fibrosis, and apoptosis, leading to heart failure (HF)[1]. Accumulating evidence has shown that cellular and extracellular non-coding RNAs (ncRNAs) participate in regulating normal physiological processes of the heart and various pathological processes of CVDs. A continued and deeper understanding of the molecular mechanisms of cellular and extracellular ncRNAs in CVDs may contribute to the development of early diagnosis and novel RNA-based therapy [2]. This special issue entitled “Cellular and Extracellular Non-coding RNAs in Cardiac Physiology and Diseases” contains ten selected papers dedicated to the role of cellular and extracellular ncRNAs on cardiovascular physiology, pathophysiology, and diseases such as ischemic heart disease, hypertension, diabetic cardiomyopathy, atherosclerosis, and vascular diseases. The roles of cellular and extracellular ncRNAs have been carefully reviewed and discussed concerning clinical diagnosis, treatment, and prognosis assessment of cardiovascular diseases. In this issue, the functions of cellular ncRNAs in CVDs were described by two groups. Zhong and Jin et al. investigated the role of microRNA (miR)-122-5p in hypertension. They proved that miR-122-5p aggravated angiotensin II-induced myocardial fibrosis and dysfunction in rats by modulating the elabela/apelin-ACE2-GDF15 signaling. Inhibition of miR-122-5p could rescue angiotensin II-induced cellular oncosis, migration, inflammation, and oxidative stress in rat cardiac fibroblasts [3]. Shan and Fang et al. investigated the function and mechanism of circular RNAs (circRNAs) in cardiac remodeling. They found that circ_0036176 inhibited mCF proliferation by translating Myo9a-208 protein to suppress the cyclin/Rb pathway [4]. This work broadened our understanding of the mechanisms underlying ncRNAs’ function in CVDs. A series of articles were then dedicated to introduce the role of extracellular ncRNAs in diabetic cardiomyopathy, atherosclerosis, vascular remodeling, and myocardial infarction. Chen et al. provided a comprehensive review of the present knowledge of how extracellular ncRNAs function in diabetic cardiomyopathy (DCM), mainly focusing on their physio-pathological properties and offering critical perspectives with respect to potential clinical translation for biomarkers and therapies [5]. Tang and Peng et al. systemically reviewed the participation of different ncRNAs in atherosclerosis (AS) in various carrier forms. They also focused on the role and potential mechanisms of extracellular ncRNAs in AS and introduced their potential implications for clinical treatment [6]. Dai et al. summarized the latest advances of extracellular ncRNAs in pathological vascular remodelingassociated diseases and described vessel-associated extracellular ncRNAs and their mechanisms of action [7]. Wang and Ding et al. provided updated information about the crosstalk mediated by extracellular circRNAs in pathological processes. They reviewed the modulation of extracellular circRNAs in ischemic myocardial injury and remodeling [8]. These articles provide the latest picture about extracellular ncRNAs as potential therapeutic targets for myocardial injury and dysfunction.