Mitochondrial regulation of obesity by POMC neurons

IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-01-19 DOI:10.1016/j.bbadis.2025.167682
Xing-dan Luo , Si Tang , Xiang-yun Luo , Luosang Quzhen , Ruo-han Xia , Xian-wang Wang
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Abstract

Pro-opiomelanocortin (POMC) neurons, nestled in the hypothalamus, play a pivotal role in the intricate coordination of energy homeostasis and metabolic pathways. These neurons' mitochondria, often hailed as the cell's powerhouses, are crucial for maintaining cellular energy equilibrium and metabolic functionality. Recent research has illuminated the complex interplay between mitochondrial dynamics and POMC neuronal activity, underscoring their critical involvement in the pathogenesis of a spectrum of metabolic disorders, notably obesity and diabetes. This comprehensive review delves into the molecular mechanisms that underlie how mitochondrial function within POMC neurons modulates metabolic regulation. We dissect the impact of mitochondrial dynamics, encompassing fusion, fission, mitophagy, and biogenesis, on the regulation of POMC neuronal activity. Furthermore, we scrutinize the role of mitochondrial dysfunction in POMC neurons in the etiology of obesity, identifying key therapeutic targets within these pathways. We offer an in-depth perspective on the indispensable role of POMC neuronal mitochondria in metabolic regulation and chart future research directions to bridge the existing knowledge gaps in this field.
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POMC神经元对肥胖的线粒体调控。
opiomelanocortin (POMC)前神经元位于下丘脑,在能量稳态和代谢途径的复杂协调中起着关键作用。这些神经元的线粒体通常被誉为细胞的“发电站”,对维持细胞能量平衡和代谢功能至关重要。最近的研究已经阐明了线粒体动力学和POMC神经元活动之间复杂的相互作用,强调了它们在一系列代谢紊乱,特别是肥胖和糖尿病的发病机制中的关键作用。这篇全面的综述深入研究了POMC神经元内线粒体功能如何调节代谢调节的分子机制。我们剖析了线粒体动力学的影响,包括融合、裂变、线粒体自噬和生物发生,对POMC神经元活动的调节。此外,我们仔细研究了POMC神经元线粒体功能障碍在肥胖病因学中的作用,确定了这些途径中的关键治疗靶点。我们对POMC神经元线粒体在代谢调节中不可或缺的作用提供了深入的视角,并绘制了未来的研究方向,以弥补该领域现有的知识空白。
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来源期刊
CiteScore
12.30
自引率
0.00%
发文量
218
审稿时长
32 days
期刊介绍: BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.
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