Noncoding RNAs and Cardiac Fibrosis

Wu, Chen; Bao, Suli; Li, Ruijie; Sun, Haofei; Peng, Yunzhu

doi:10.31083/j.rcm2402063

Cited by 3 publications

(2 citation statements)

References 78 publications

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“…Inhibition of MALAT1 can increase the protein expression level of NRF2/SLC7A11 in myocardial infarction models, both in vitro and in vivo , while reducing ferrous ion levels and lipid peroxidation in cells. This implies that MALAT1 represents a promising target for the prevention and treatment of AMI [ 41 , 42 ].…”

Section: Ferroptosis and Lipid Peroxidation In Amimentioning

confidence: 99%

Ferroptosis and Lipid Metabolism in Acute Myocardial Infarction

Wu,

Li,

Cheng

et al. 2024

Rev. Cardiovasc. Med.

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Acute myocardial infarction (AMI) is triggered by the blockage of coronary arteries, leading to restricted blood flow to the myocardium, which results in damage and cell death. While the traditional understanding of cell death primarily revolves around apoptosis, a new player in the game has emerged: ferroptosis. This novel form of cell death relies on iron and is propelled by reactive oxygen species (ROS). Lipid metabolism, an indispensable physiological process, plays a vital role in preserving cellular homeostasis. However, when this metabolic pathway is disrupted, the accumulation of excess waste increases, specifically lipid peroxides, which are strongly linked to the occurrence and progression of AMI. As a result, comprehending this complex interaction between ferroptosis and lipid metabolism could pave the way for new therapeutic approaches in tackling AMI.

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Section: Ferroptosis and Lipid Peroxidation In Amimentioning

confidence: 99%

Ferroptosis and Lipid Metabolism in Acute Myocardial Infarction

Wu,

Li,

Cheng

et al. 2024

Rev. Cardiovasc. Med.

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“…For instance, the lncRNA LICPAR has been identified as a promoter of AF development through its regulation of the TGF-β/Smad signaling pathway [81]. Additionally, increased expression of MALAT1 has been observed in AF patients and is implicated in the development of AF by modulating apoptosis and cardiomyocyte superoxide dismutase expression, among other mechanisms [82]. Another lncRNA, ANRIL, which is associated with cardiovascular disease, exhibits upregulated expression in AF patients and can influence the onset and progression of AF by affecting the expression of ion channels, among other pathways [83,84].…”

Section: Atrial Fibrillation (Af)mentioning

confidence: 99%

Review:Research status of cardiovascular and cerebrovascular diseases and non-coding RNA

Jiang¹,

Hu²

2023

Clin. transl. rep.

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Cardiovascular and cerebrovascular diseases (CVD) encompass a range of conditions affecting the heart, brain, and blood vessels, including coronary heart disease, hypertension, and stroke. In recent years, there has been growing evidence highlighting the significant role of non-coding RNAs (ncRNAs) in the development and progression of cardiovascular diseases. Among the various types of ncRNAs, long-stranded non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) have emerged as prominent players in cardiovascular research. Advancements in technology and in-depth research have revealed that ncRNAs and circRNAs exert regulatory effects on the biological functions of the cardiovascular system through various pathways. For instance, they can modulate the proliferation, migration, and apoptosis of vascular endothelial cells, as well as regulate cardiac muscle contraction and cardiomyocyte apoptosis. Additionally, ncRNAs and circRNAs can influence downstream targets and pathways involved in cardiovascular diseases. The exploration of ncRNAs and circRNAs in cardiovascular research has opened up new avenues for the diagnosis and treatment of CVDs. By understanding the intricate regulatory mechanisms mediated by these non-coding RNAs, researchers have gained valuable insights into the pathogenesis of cardiovascular diseases and identified potential therapeutic targets. Consequently, these studies have provided novel ideas and approaches for the diagnosis, prevention, and management of CVDs.

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