سامانه همایش های دانشگاه آزاد اسلامی واحد نجف آباد

صفحه اصلی / اولین همایش بین المللی تحول خدمات سلامت: تلفیق مراقبت، درمان، بازتوانی و امیدبخشی

Inflammaging and Functional Decline in Aging: Immunological Links to Sarcopenia, Frailty, and Disability and the Role of Lifestyle and Rehabilitation Interventions

نویسندگان :

Nasrin Zare¹ Fatemeh Hadian²

1- دانشگاه آزاد اسلامی واحد نجف آباد ، اصفهان 2- دانشگاه آزاد اسلامی واحد نجف آباد ، اصفهان

کلمات کلیدی :

Inflammaging،cytokines،sarcopenia،frailty،disability،exercise،nutrition،rehabilitation

چکیده :

Background: Recent research has identified inflammaging, a chronic low grade systemic inflammatory state associated with aging, as a common biological denominator and a central pathological axis underlying age related syndromes such as sarcopenia, frailty, and disability (1–3). This inflammatory state disrupts muscle protein homeostasis through multiple mechanisms, including the accumulation of senescent cells exhibiting a senescence associated secretory phenotype (SASP), mitochondrial dysfunction characterized by increased production of reactive oxygen species (ROS) and release of mitochondrial DNA (mtDNA), and immunosenescence manifested by alterations in T cell subsets and reduced CD28 expression (4–6). Collectively, these processes impair anabolic signaling, leading to anabolic resistance, muscle atrophy, and depletion of physiological reserves. Moreover, systemic inflammation contributes to inflammatory anemia, endothelial dysfunction, and neuroinflammation, thereby increasing vulnerability to frailty and disability (4,7–9). Finding: Evidence indicates that non pharmacological interventions play a pivotal role in modulating inflammaging. Structured exercise programs, particularly progressive resistance training and multimodal interventions, reduce pro inflammatory cytokines such as IL 6 and TNF α while enhancing mitochondrial biogenesis, resulting in improved muscle function (10–12). In addition, targeted nutritional strategies, including increasing protein intake to 1.2–1.5 g/kg/day, evenly distributing protein across meals (25–30 g per meal), adherence to the Mediterranean dietary pattern, and supplementation with omega 3 fatty acids and vitamin D, effectively counteract inflammatory burden (13–16). Furthermore, recognizing the exacerbating role of chronic comorbidities such as chronic kidney disease (CKD) and chronic obstructive pulmonary disease (COPD), alongside advanced rehabilitation and cytokine modulating approaches targeting pathways such as IL 18 and IL 37, is essential for developing personalized interventions (3,17,18). Conclusion: Inflammaging represents a central biological mechanism driving anabolic resistance, sarcopenia, frailty, and disability in aging populations (1–4). Current evidence supports the effectiveness of exercise and targeted nutritional strategies in interrupting this detrimental inflammatory cycle. Moreover, emerging therapeutic approaches, including senotherapy (senolytics) and mesenchymal stem cell based therapies, offer promising future avenues for reversing functional decline and promoting healthy aging (3,19). Keywords: Inflammaging; cytokines; sarcopenia; frailty; disability; exercise; nutrition; rehabilitation.