Abstract

COVID-19 severe symptoms and high mortality are mainly seen in elders with age-associated diseases who have mitochondrial dysfunction. Mitochondrial dysfunction is a vulnerability and comorbidity of COVID-19. Cytokine storm, and increased serum iron and ferritin and reactive oxygen species (ROS) in COVID-19 further damage mitochondria. Amelioration of mitochondrial dysfunction may be a strategy of prevention and treatment of COVID-19. We also describe mitochondrial organelle transplantation (MOT) which has restored mitochondrial function, improved the repair of injured tissues and suppressed hyperinflammation in life-threatening sepsis. MOT is a potential therapy for severe COVID-19. Finally, we report the first case of MOT for a severe COVID-19 patient. MOT is safe and might have beneficial effect on the severe COVID-19.

Highlights

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an enveloped RNA betacoronavirus that causes coronavirus disease 2019 (COVID-19)

  • Improvement of mitochondrial activity in the elders would serve as preventive strategy to improve the immune response and reduce mortality caused by COVID-19 and other viral respiratory diseases such as influenza [9]

  • Mesenchymal stem cells (MSCs) lack angiotensin-converting enzyme-2 (ACE2) receptor, which is a receptor widely distributed on the surface of human cells and required for the entry of coronavirus into host cells

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Summary

Introduction

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an enveloped RNA betacoronavirus that causes coronavirus disease 2019 (COVID-19). Morris G. et al proposed a model of pathophysiological processes of COVID-19 starting from the infection of human type II alveolar epithelial cells (pneumocytes) by SARS-CoV-2 and culminating in the development of ARDS. Activated macrophages secrete proinflammatory cytokines and chemokines which further activate vascular endothelial cells and recruit highly toxic neutrophils and inflammatory activated platelets into the alveolar space. These activated cells and platelets further produce proinflammatory cytokines and reactive oxygen species (ROS) and contribute to the development of coagulopathy, systemic sepsis, a cytokine storm, ARDS and collapsed lungs [8]. We will report the first case of MOT therapy for a severe COVID-19 patient. The MOT is safe for the patient who might gain some benefit from the MOT therapy

Mitochondrial Dysfunction Often Pre-Exists in Patients with Severe COVID-19
SARS-CoV-2 May Directly Damage Human Mitochondria
ROS Accumulation in COVID-19
Elevated Serum Iron and Ferritin
Damage of Extracellular Mitochondria
Mitochondrial Transfer between Cells
MOT with Isolated Mitochondria
Exogenous Mitochondria Have Immunomodulatory Effect
Case Report
Findings
Summary and Conclusion
Full Text
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