The global rise in obesity and population aging represents a major public health challenge, with growing evidence suggesting that excess body fat not only increases the risk of chronic disease but may also accelerate the biological aging process. A new review examines the close relationship between obesity and aging, highlighting the overlapping molecular mechanisms that link the two conditions and exploring whether anti-obesity therapies could help slow aging and reduce age-related disease.
The review explains that aging is driven by multiple biological hallmarks, including chronic inflammation, telomere shortening, mitochondrial dysfunction, genomic instability, impaired protein homeostasis, stem cell exhaustion, and altered nutrient sensing. Obesity appears to promote many of these same changes, suggesting that it acts as an accelerator of biological aging rather than simply increasing disease risk independently.
One of the strongest links between obesity and aging is chronic low-grade inflammation. Excess adipose tissue becomes infiltrated by immune cells that produce inflammatory cytokines, creating persistent systemic inflammation that contributes to insulin resistance, metabolic dysfunction, cardiovascular disease, and tissue damage. According to the review, this inflammatory state closely resembles the phenomenon of “inflammaging” observed during normal aging.
The authors also describe several additional mechanisms through which obesity may accelerate aging, including telomere depletion, epigenetic alterations, mitochondrial dysfunction, stem cell exhaustion, genomic instability, protein homeostasis disruption, cellular senescence, and gut microbiome dysbiosis. A summary diagram in the review illustrates these ten interconnected processes, emphasizing how obesity affects many of the same biological pathways that naturally deteriorate with age.
The review highlights evidence that weight loss interventions may partially reverse some of these aging-related changes. Lifestyle approaches such as calorie restriction and exercise, together with pharmacological treatments and bariatric surgery, have been associated with improvements in metabolic function and reductions in biological markers linked to aging. In particular, modern anti-obesity medications—including liraglutide, semaglutide, tirzepatide, and orlistat—are discussed for their potential to improve healthy lifespan by reducing inflammation, improving mitochondrial function, enhancing telomerase activity, and limiting oxidative stress.
# # # # # #
Genes & Diseases publishes rigorously peer-reviewed and high quality original articles and authoritative reviews that focus on the molecular bases of human diseases. Emphasis is placed on hypothesis-driven, mechanistic studies relevant to pathogenesis and/or experimental therapeutics of human diseases. The journal has worldwide authorship, and a broad scope in basic and translational biomedical research of molecular biology, molecular genetics, and cell biology, including but not limited to cell proliferation and apoptosis, signal transduction, stem cell biology, developmental biology, gene regulation and epigenetics, cancer biology, immunity and infection, neuroscience, disease-specific animal models, gene and cell-based therapies, and regenerative medicine.
Scopus CiteScore: 10.4 |Impact Factor:14.6
# # # # # #
More information: https://www.keaipublishing.com/en/journals/genes-and-diseases/
Editorial Board: https://www.keaipublishing.com/en/journals/genes-and-diseases/editorial-board/
All issues and articles in press are available online in ScienceDirect (https://www.sciencedirect.com/journal/genes-and-diseases).
Submissions to Genes & Diseases may be made using Editorial Manager (https://www.editorialmanager.com/gendis/default.aspx).
Print ISSN: 2352-4820
eISSN: 2352-3042
CN: 50-1221/R
Contact Us: editor@genesndiseases.cn
X (formerly twitter): @GenesNDiseases (https://x.com/GenesNDiseases)
# # # # # #
Reference
Rui Zhang, Linlin Liu, Xiaoman Shi, Yanming Ren, Obesity accelerates aging: Mechanisms and therapeutic implications, Genes & Diseases, Volume 13, Issue 5, 2026, 101980, https://doi.org/10.1016/j.gendis.2025.101980

Funding
National Natural Science Foundation of China 82302627
National Natural Science Foundation of China 82472683