{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMT‐ND5 is a mitochondrially encoded subunit of respiratory complex I that plays a pivotal role in coupling NADH oxidation to proton translocation and thus in ATP synthesis. Functional studies have demonstrated that missense mutations in MT‐ND5—such as a V253A change that disrupts complex I assembly, a mutation that impairs mitochondrial calcium uptake, and alterations identified in animal models—compromise electron transport and mitochondrial membrane potential, thereby perturbing cellular bioenergetics."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nA broad spectrum of pathogenic variants in MT‐ND5 has been identified in human mitochondrial disorders. Heteroplasmic and homoplasmic mutations in this gene have been linked to diseases such as Leber hereditary optic neuropathy, MELAS, Leigh syndrome, hypertrophic cardiomyopathy, exercise intolerance, and maternally inherited diabetes with retinopathy. These mutations disrupt complex I activity—diminishing electron flow, reducing ATP production, and ultimately leading to multisystem clinical manifestations. The accumulation of various MT‐ND5 mutations also highlights its status as a mutational hotspot underlying diverse phenotypes ranging from neurologic and neuromuscular disease to cardiac dysfunction and even tumor cell adaptations."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAlterations in MT‐ND5 are also increasingly implicated in neuropsychiatric and stress‐related disorders. Specific low‐frequency and amino acid–changing ND5 variants have been associated with idiopathic Parkinson’s disease, schizophrenia, bipolar disorder, and posttraumatic stress disorder, suggesting that even subtle perturbations of MT‐ND5 function can impact neuronal bioenergetics, redox balance, and intracellular signaling. Moreover, studies in tumor cell models have revealed that adaptive transcriptional upregulation may mitigate the functional impact of ND5 mutations, while cytoplasmic p53 signaling can modulate complex I activity via interactions with ND5 to regulate reactive oxygen species production and cell invasiveness."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "28"}, {"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its coding capacity, non‐coding transcripts derived from the MT‐ND5 locus—such as a circular RNA (circMTND5)—have emerged as novel regulators of mitochondrial gene expression. In models of lupus nephritis, circMTND5 appears to mitigate mitochondrial dysfunction and tissue fibrosis by sequestering specific microRNAs, thereby unveiling a new layer of post‐transcriptional control over mitochondrial homeostasis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "H G Bao, C J Zhao, J Y Li, et al. 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