NAD+ Metabolism in Aging and Cancer

IF 4.7 2区 医学 Q1 ONCOLOGY
T. Demarest, M. Babbar, M. Okur, Xiuli Dan, D. Croteau, Nima B Fakouri, M. Mattson, V. Bohr
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引用次数: 41

Abstract

Aging is a major risk factor for many types of cancer, and the molecular mechanisms implicated in aging, progeria syndromes, and cancer pathogenesis display considerable similarities. Maintaining redox homeostasis, efficient signal transduction, and mitochondrial metabolism is essential for genome integrity and for preventing progression to cellular senescence or tumorigenesis. NAD+ is a central signaling molecule involved in these and other cellular processes implicated in age-related diseases and cancer. Growing evidence implicates NAD+ decline as a major feature of accelerated aging progeria syndromes and normal aging. Administration of NAD+ precursors such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) offer promising therapeutic strategies to improve health, progeria comorbidities, and cancer therapies. This review summarizes insights from the study of aging and progeria syndromes and discusses the implications and therapeutic potential of the underlying molecular mechanisms involved in aging and how they may contribute to tumorigenesis.
衰老与癌症中的NAD+代谢
衰老是许多类型癌症的主要危险因素,与衰老、早衰综合征和癌症发病机制相关的分子机制显示出相当大的相似性。维持氧化还原稳态、有效的信号转导和线粒体代谢对于基因组完整性和防止细胞衰老或肿瘤发生至关重要。NAD+是一种中枢信号分子,参与与年龄相关疾病和癌症相关的这些和其他细胞过程。越来越多的证据表明NAD+下降是加速衰老早衰综合征和正常衰老的主要特征。NAD+前体如烟酰胺核苷(NR)和烟酰胺单核苷酸(NMN)的管理为改善健康、早衰合并症和癌症治疗提供了有希望的治疗策略。本文综述了衰老和早衰综合征的研究成果,并讨论了衰老的潜在分子机制及其对肿瘤发生的影响和治疗潜力。
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
CiteScore
14.50
自引率
1.30%
发文量
13
期刊介绍: The Annual Review of Cancer Biology offers comprehensive reviews on various topics within cancer research, covering pivotal and emerging areas in the field. As our understanding of cancer's fundamental mechanisms deepens and more findings transition into targeted clinical treatments, the journal is structured around three main themes: Cancer Cell Biology, Tumorigenesis and Cancer Progression, and Translational Cancer Science. The current volume of this journal has transitioned from gated to open access through Annual Reviews' Subscribe to Open program, ensuring all articles are published under a CC BY license.
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