One notable challenge with xenomitochondrial and conplastic mtDNA models lies in the potential for heteroplasmythe intercellular coexistence of wild-type and mutant (nDNA and/or mtDNA) strands
Collectively, insulin resistance represents a central pathophysiological nexus in CMS, linking dysregulated glucose and lipid metabolism, chronic inflammation, and endothelial dysfunction (73, 74)
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