Long Non-Coding RNAs as Modulators of Metabolic Reprogramming for Endogenous Heart Regeneration: Mechanisms and Therapeutic Potential.

IF 4.4 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biomedical Journal Pub Date : 2025-09-15 DOI:10.1016/j.bj.2025.100914

Xueping Wu, Yehui Lv, Zhihong Li, Zhifang Yang

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引用次数: 0

Abstract

Myocardial infarction (MI) is one of the leading causes of death worldwide, with its high incidence and mortality posing a significant threat to human health. Despite some progress in the treatment of myocardial infarction, mortality rates remain alarmingly high. Adult mammals have limited myocardial regenerative capacity, and extensive cell death caused by myocardial ischemia severely impairs cardiac function, leading to heart failure or death. In contrast, neonatal myocardium possesses a robust regenerative ability, which gradually diminishes after birth. The loss of cardiomyocyte regenerative capacity is often accompanied by a shift in energy metabolism-from reliance on glucose (glycolysis) to fatty acid oxidation. This metabolic reprogramming significantly impacts CM proliferation. Long non-coding RNAs (lncRNAs) orchestrate cardiac regeneration through epigenetic control (e.g., Bvht/PRC2-mediated silencing), metabolic reprogramming (e.g., GATA6-AS1 suppression of FAO), and miRNA sponging (e.g., CAREL sequestration of miR-296). However, our understanding of the metabolic determinants and pathways that promote myocardial regeneration after myocardial infarction is still insufficient. This review investigates the interplay between lncRNAs and metabolic reprogramming in cardiovascular function, aiming to identify novel therapeutic targets and strategies to enhance myocardial regeneration post-MI.

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长链非编码rna作为内源性心脏再生代谢重编程的调节剂：机制和治疗潜力。

心肌梗死（MI）是世界范围内导致死亡的主要原因之一，其高发病率和死亡率对人类健康构成重大威胁。尽管在治疗心肌梗塞方面取得了一些进展，但死亡率仍然高得惊人。成年哺乳动物的心肌再生能力有限，心肌缺血引起的广泛细胞死亡严重损害心功能，导致心力衰竭或死亡。相反，新生儿心肌具有强大的再生能力，但在出生后逐渐减弱。心肌细胞再生能力的丧失通常伴随着能量代谢的转变——从依赖葡萄糖（糖酵解）到脂肪酸氧化。这种代谢重编程显著影响CM增殖。长链非编码rna （lncRNAs）通过表观遗传控制（如Bvht/ prc2介导的沉默）、代谢重编程（如GATA6-AS1对FAO的抑制）和miRNA海绵（如miR-296的CAREL隔离）来协调心脏再生。然而，我们对心肌梗死后促进心肌再生的代谢决定因素和途径的理解仍然不足。本文综述了lncrna与心血管功能代谢重编程之间的相互作用，旨在寻找新的治疗靶点和策略来增强心肌梗死后的心肌再生。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Biomedical Journal Medicine-General Medicine

CiteScore

11.60

自引率

1.80%

发文量

128

审稿时长

42 days

期刊介绍： Biomedical Journal publishes 6 peer-reviewed issues per year in all fields of clinical and biomedical sciences for an internationally diverse authorship. Unlike most open access journals, which are free to readers but not authors, Biomedical Journal does not charge for subscription, submission, processing or publication of manuscripts, nor for color reproduction of photographs. Clinical studies, accounts of clinical trials, biomarker studies, and characterization of human pathogens are within the scope of the journal, as well as basic studies in model species such as Escherichia coli, Caenorhabditis elegans, Drosophila melanogaster, and Mus musculus revealing the function of molecules, cells, and tissues relevant for human health. However, articles on other species can be published if they contribute to our understanding of basic mechanisms of biology. A highly-cited international editorial board assures timely publication of manuscripts. Reviews on recent progress in biomedical sciences are commissioned by the editors.