Louay Abo Qoura , Alexey V. Churov , Olga N. Maltseva , Mikhail S. Arbatskiy , Olga N. Tkacheva
{"title":"衰老相互作用:从细胞失调到年龄相关疾病的治疗前沿","authors":"Louay Abo Qoura , Alexey V. Churov , Olga N. Maltseva , Mikhail S. Arbatskiy , Olga N. Tkacheva","doi":"10.1016/j.bbadis.2025.168060","DOIUrl":null,"url":null,"abstract":"<div><div>Biological aging is a complex, multifaceted process characterized by the progressive erosion of cellular homeostasis, driven by intersecting pathways of inflammaging, immune senescence, mitochondrial dysfunction, and genomic instability. This review delineates current knowledge on the interconnected mechanisms underlying aging-related diseases, including atherosclerosis, obesity, sarcopenia, neurodegenerative disorders, rheumatoid arthritis, and cancer. We further discuss the critical role of contributing factors such as microbiome dysbiosis, sex differences, and exosome-mediated communication in modulating disease progression. Advancements in multi-omics technologies and AI-driven biomarkers, particularly epigenetic clocks, are highlighted for their ability to precisely quantify biological aging and stratify disease risk. Finally, we explore the therapeutic potential and promising clinical trials of targeting these shared mechanisms with senolytics, mitochondrial enhancers, and immunomodulators, offering a paradigm shift from disease-specific treatment to holistic interventions designed to extend healthspan.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1872 1","pages":"Article 168060"},"PeriodicalIF":4.2000,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The aging interactome: From cellular dysregulation to therapeutic frontiers in age-related diseases\",\"authors\":\"Louay Abo Qoura , Alexey V. Churov , Olga N. Maltseva , Mikhail S. Arbatskiy , Olga N. Tkacheva\",\"doi\":\"10.1016/j.bbadis.2025.168060\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Biological aging is a complex, multifaceted process characterized by the progressive erosion of cellular homeostasis, driven by intersecting pathways of inflammaging, immune senescence, mitochondrial dysfunction, and genomic instability. This review delineates current knowledge on the interconnected mechanisms underlying aging-related diseases, including atherosclerosis, obesity, sarcopenia, neurodegenerative disorders, rheumatoid arthritis, and cancer. We further discuss the critical role of contributing factors such as microbiome dysbiosis, sex differences, and exosome-mediated communication in modulating disease progression. Advancements in multi-omics technologies and AI-driven biomarkers, particularly epigenetic clocks, are highlighted for their ability to precisely quantify biological aging and stratify disease risk. Finally, we explore the therapeutic potential and promising clinical trials of targeting these shared mechanisms with senolytics, mitochondrial enhancers, and immunomodulators, offering a paradigm shift from disease-specific treatment to holistic interventions designed to extend healthspan.</div></div>\",\"PeriodicalId\":8821,\"journal\":{\"name\":\"Biochimica et biophysica acta. Molecular basis of disease\",\"volume\":\"1872 1\",\"pages\":\"Article 168060\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2025-09-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biochimica et biophysica acta. Molecular basis of disease\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0925443925004089\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochimica et biophysica acta. Molecular basis of disease","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0925443925004089","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
The aging interactome: From cellular dysregulation to therapeutic frontiers in age-related diseases
Biological aging is a complex, multifaceted process characterized by the progressive erosion of cellular homeostasis, driven by intersecting pathways of inflammaging, immune senescence, mitochondrial dysfunction, and genomic instability. This review delineates current knowledge on the interconnected mechanisms underlying aging-related diseases, including atherosclerosis, obesity, sarcopenia, neurodegenerative disorders, rheumatoid arthritis, and cancer. We further discuss the critical role of contributing factors such as microbiome dysbiosis, sex differences, and exosome-mediated communication in modulating disease progression. Advancements in multi-omics technologies and AI-driven biomarkers, particularly epigenetic clocks, are highlighted for their ability to precisely quantify biological aging and stratify disease risk. Finally, we explore the therapeutic potential and promising clinical trials of targeting these shared mechanisms with senolytics, mitochondrial enhancers, and immunomodulators, offering a paradigm shift from disease-specific treatment to holistic interventions designed to extend healthspan.
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.