Advances in mitochondrial inflammatory damage in depression

Depression, as a typical mood disorder, is characterized by high prevalence, recurrence, disability and suicide rates, and its core pathological mechanism involves cytokine disorders and neuroimmune homeostatic imbalance. Studies have shown that the central nervous system and peripheral immune system can activate immune cells to release proinflammatory factors under stressful stimuli, which induces pathological processes such as impaired synaptic remodeling, blocked neuronal regeneration, and aberrant apoptosis, and ultimately leads to impaired neuroplasticity. As the energy metabolism center of eukaryotic cells, mitochondria play a pivotal role in neurogenesis, apoptosis regulation and synaptic plasticity. Recent studies have proposed the "inflammation-mitochondrial damage" vicious cycle hypothesis, which suggests that mitochondrial dysfunction mediated by inflammatory factors can exacerbate the neuroinflammatory response, and that mitochondrial dysfunction regulation may be a key target to interrupt this vicious cycle. In this paper, we systematically analyze the damage mechanisms of the inflammatory microenvironment on mitochondrial structure and function, and deeply analyze the intrinsic association between abnormal mitochondrial dynamics and the occurrence and development of depression, with the aim of providing a new theoretical basis and intervention strategy for the precise prevention and treatment of depression.