The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has introduced the medical
community to the phenomenon of long COVID, a condition characterized by persistent
symptoms following the resolution of the acute phase of infection. Among the myriad
of symptoms reported by long COVID sufferers, chronic fatigue, cognitive disturbances,
and exercise intolerance are predominant, suggesting systemic alterations beyond the
initial viral pathology. Emerging evidence has pointed to mitochondrial dysfunction
as a potential underpinning mechanism contributing to the persistence and diversity
of long COVID symptoms. This review aims to synthesize current findings related to
mitochondrial dysfunction in long COVID, exploring its implications for cellular energy
deficits, oxidative stress, immune dysregulation, metabolic disturbances, and endothelial
dysfunction. Through a comprehensive analysis of the literature, we highlight the
significance of mitochondrial health in the pathophysiology of long COVID, drawing
parallels with similar clinical syndromes linked to post-infectious states in other
diseases where mitochondrial impairment has been implicated. We discuss potential
therapeutic strategies targeting mitochondrial function, including pharmacological
interventions, lifestyle modifications, exercise, and dietary approaches, and emphasize
the need for further research and collaborative efforts to advance our understanding
and management of long COVID. This review underscores the critical role of mitochondrial
dysfunction in long COVID and calls for a multidisciplinary approach to address the
gaps in our knowledge and treatment options for those affected by this condition.
