Exploring the Network between Adipocytokines and Inflammatory Response in SARS-CoV-2 Infection: A Scoping Review

Abstract

Adipose tissue is actually regarded as an endocrine organ, rather than as an organ that merely stores energy. During the COVID-19 pandemic, obesity has undoubtedly emerged as one of the most important risk factors for disease severity and poor outcomes related to SARS-CoV-2 infection. The aberrant production of cytokine-like hormones, called adipokines, may contribute to alterations in metabolism, dysfunction in vascular endothelium and the creation of a state of general chronic inflammation. Moreover, chronic, low-grade inflammation linked to obesity predisposes the host to immunosuppression and excessive cytokine activation. In this respect, understanding the mechanisms that link obesity with the severity of SARS-CoV-2 infection could represent a real game changer in the development of new therapeutic strategies. Our review therefore examines the pathogenic mechanisms of SARS-CoV-2, the implications with visceral adipose tissue and the influences of the adipose tissue and its adipokines on the clinical behavior of COVID-19.

Keywords: COVID-19; SARS-CoV-2; adipocytokines; adiponectin; leptin.

Figure 1

Difference between visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT).

Figure 2

Pathogenic mechanisms of SARS-CoV-2 infection. ACE2: angiotensin-converting enzyme 2; S Protein: spike protein; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; TMPRSS2: transmembrane protease serine 2.

Figure 3

Postulated implications of obesity during SARS-CoV-2 infection. ACE-2: angiotensin-converting enzyme 2; ALI: acute lung injury; ARDS: acute respiratory distress syndrome; IL-6: interleukin 6; TNF-α: tumor necrosis factor alpha. Arrows indicate induced responses.