Reviving the mutual impact of SARS-COV-2 and obesity on patients: From morbidity to mortality.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Obesity-related metabolic dysfunction, endothelium imbalance, chronic inflammation, immune dysregulation, and its comorbidities may all have a role in systemic inflammation, leading to the pulmonary fibrosis and cytokine storm, which leads to failure of lung function, which is a hallmark of severe SARS-CoV-2 infection. Obesity may also disrupt the function of mucociliary escalators and cooperation of epithelial cell's motile cilia in the airway, limiting the clearance of the coronavirus that causes severe acute respiratory syndrome (SARS-CoV-2). Adipose tissues in obese patients have a greater number of proteases and receptors for SARS-CoV-2 admittance, proposing that they could serve as an accelerator and reservoir for this virus, boosting immunological response and systemic inflammation. Lastly, anti-inflammatory cytokines such as anti-IL-6 and the infusion of mesenchymal stem cells could be used as a modulation therapy of immunity to help COVID-19 patients. Obesity, on the other hand, is linked to the progress of COVID-19 through a variety of molecular pathways, and obese people are part of the SARS-CoV-2 susceptible individuals, necessitating more protective measures.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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