Mechanism of PI3K/Akt‑mediated mitochondrial pathway in obesity‑induced apoptosis (Review).

Abstract

Obesity is a pervasive global health challenge that substantially reduces the quality of life of millions of individuals and impedes social and economic advancement. Obesity is an independent risk factor that contributes to a range of chronic non-communicable metabolic diseases, significantly affecting energy metabolism, mental health, cancer susceptibility, sleep quality, and other physiological processes. The PI3K/AKT signaling pathway, a significant glucose, lipid, and protein metabolism regulator, is integral to cellular growth, survival, and apoptosis. Apoptosis is a highly regulated form of programmed cell death that is critical for immune cell maturation and tissue repair. The present review examines the association between obesity, the PI3K/AKT pathway, and mitochondrial apoptosis to elucidate the potential mechanisms by which obesity may activate apoptotic pathways. These findings provide a theoretical foundation for mitigating obesity-related complications by targeting these critical pathways.