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When cardiolipin becomes oxidized, it migrates to the outer membrane, where it can interact with cytoplasmic amyloidogenic proteins to facilitate the formation of pores in the mitochondrial membrane, and, ultimately, to trap mitochondrial debris from aged mitochondria within fibrillar extracellular deposits such as Lewy bodies (Seneff et al., 2025b)

Studies show persistent elevation of vascular injury markers such as vWF and cytokines, suggesting ongoing thromboinflammation and hypercoagulable states in Long COVID [362, 363]

Am J Physiol 1990