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Some studies have suggested that SARS-CoV-2 could influence mitochondrial function directly or indirectly in multiple mechanisms involving angiotensin-converting enzyme 2 (ACE-2), transmembrane serine protease 2 (TMPRSS2) [235], innate immunity functions [238]

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This genetic anomaly in MeCbl synthesis leads to the accumulation of homocysteine, a condition termed hyperhomocysteinemia or homocystinuria [94, 100], (Fig