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. 2024 May 24;22:285. doi: 10.1186/s12964-024-01663-1

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Aging drivers and age-related diseases. Major physiological features of aging include NAD⁺ loss, telomeres attrition, mitochondrial dysfunction, stem cell exhaustion, disabled macro-autophagy, DNA damage, protein balance loss, inflammation, dysbiosis, deregulated nutrient sensing, and altered cellular communication. These physiological characteristics of aging are primitive, antagonistic, and integrated, and their interaction promotes aging. When aging reaches a certain threshold, organ and tissue function continues to deteriorate, which increases the incidence and mortality of aging-related diseases, including cardiovascular, cerebrovascular, degenerative joint disease, diabetes, Parkinson’s disease, Alzheimer’s disease, and cancer