Mitochondrial dynamic changes and energy surplus

Mitochondrial homeostasis is essential for cell survival and metabolic balance. This review systematically examines the molecular mechanisms, pathological correlations, and regulatory relationships among three major processes: mitochondrial homeostasis, lipoacylation modification, and mitochondrial overheating (excess energy). Mitochondrial dynamic balance adapts to energy demands through division mediated by Drp1, as well as regulation by Mfn1/2 and OPA1 for fusion. lipoacylation activates PDH and α-KGDHC, which ensures metabolic efficiency and reduces ROS. Overheating characterized by increased ATP/ADP ratios, an enhanced ETC reducing state, and ROS accumulation, disrupts the first two processes and creates a vicious cycle. This network disorder is a common pathological basis for neurodegenerative diseases (such as CMT2A, AD), cardiovascular diseases (such as dilated cardiomyopathy), and metabolic diseases (such as type 2 diabetes and NAFLD). However, the details of these sensing pathways regulation remain unclear and require further investigation. This review aims to provide a theoretical framework for researching and treating diseases related to mitochondrial dysfunction.