IL-17A and TNF-α as potential biomarkers for acute respiratory distress syndrome and mortality in patients with obesity and COVID-19

Leija-Martínez, José J.; Huang, Fengyang; Del-Río-Navarro, Blanca E.; Sánchez‐Muñoz, Fausto; Muñoz‐Hernández, Onofre; Giacoman-Martínez, Abraham; Hall-Mondragon, Margareth S.; Espinosa-Velazquez, Dario

doi:10.1016/j.mehy.2020.109935

Cited by 49 publications

(59 citation statements)

References 45 publications

(51 reference statements)

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“…Chronic elevations of pro-inflammatory cytokines, such as TNF-α and IL-6, also directly influence COVID-19 disease course. Because TNF-α plays an important role in promoting ARDS, obese individuals with chronically elevated serum TNF-α are at greater risk of developing this life-threatening complication [ 102 ]. In patients with COVID-19, IL-6 levels are significantly elevated and associated with adverse clinical outcomes.…”

Section: Underlying Mechanisms Linking Obesity To Major Complications As a Results Of Sars-cov-2 Infectionmentioning

confidence: 99%

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

Demeulemeester¹,

Punder²,

Heijningen³

et al. 2021

Cells

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Emerging data suggest that obesity is a major risk factor for the progression of major complications such as acute respiratory distress syndrome (ARDS), cytokine storm and coagulopathy in COVID-19. Understanding the mechanisms underlying the link between obesity and disease severity as a result of SARS-CoV-2 infection is crucial for the development of new therapeutic interventions and preventive measures in this high-risk group. We propose that multiple features of obesity contribute to the prevalence of severe COVID-19 and complications. First, viral entry can be facilitated by the upregulation of viral entry receptors, like angiotensin-converting enzyme 2 (ACE2), among others. Second, obesity-induced chronic inflammation and disruptions of insulin and leptin signaling can result in impaired viral clearance and a disproportionate or hyper-inflammatory response, which together with elevated ferritin levels can be a direct cause for ARDS and cytokine storm. Third, the negative consequences of obesity on blood coagulation can contribute to the progression of thrombus formation and hemorrhage. In this review we first summarize clinical findings on the relationship between obesity and COVID-19 disease severity and then further discuss potential mechanisms that could explain the risk for major complications in patients suffering from obesity.

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Section: Underlying Mechanisms Linking Obesity To Major Complications As a Results Of Sars-cov-2 Infectionmentioning

confidence: 99%

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

Demeulemeester¹,

Punder²,

Heijningen³

et al. 2021

Cells

View full text Add to dashboard Cite

show abstract

“…Since serum concentration of TNF-α is elevated in COVID-19 patients [ 31 ], and also during low-grade chronic inflammation in the obese, inflammation and thrombosis could both be attributed to the increased TNF-α activity. Therefore, serum TNF-α could be considered as potential biomarker in acute respiratory distress syndrome (ARDS) in obese COVID-19 patients [ 32 ], and thus can be targeted to control the severity of the disease.…”

Section: Mediators Of Inflammationmentioning

confidence: 99%

COVID-19 severity in obese patients: Potential mechanisms and molecular targets for clinical intervention

Sharma

Yadav

2021

Obesity Research & Clinical Practice

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“…In this study, we found that Quercetin is capable of binding with the active site of ACE2 by forming conventional hydrogen bond and Pi-Alkyl interactions with amino acids TRP 69 , LEU 391 , LEU 73 and ALA 99 . Besides, the activation of TNF and NF-кB signaling pathways were identified as the novel changes in the pathogenesis of COVID-19 [ 57 – 59 ]. Our data from network pharmacology also suggested that five signaling pathways including TNF, HIF-1α, TLR, apoptosis-related, and VEGF signaling may be the therapeutic pathways in Quercetin treatment to COVID-19-induced AKI.…”

Section: Discussionmentioning

confidence: 99%

Quercetin as a potential treatment for COVID-19-induced acute kidney injury: Based on network pharmacology and molecular docking study

Zhang

Cen

et al. 2021

PLoS ONE

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Kidneys are one of the targets for SARS-CoV-2, it is reported that up to 36% of patients with SARS-CoV-2 infection would develop into acute kidney injury (AKI). AKI is associated with high mortality in the clinical setting and contributes to the transition of AKI to chronic kidney disease (CKD). Up to date, the underlying mechanisms are obscure and there is no effective and specific treatment for COVID-19-induced AKI. In the present study, we investigated the mechanisms and interactions between Quercetin and SARS-CoV-2 targets proteins by using network pharmacology and molecular docking. The renal protective effects of Quercetin on COVID-19-induced AKI may be associated with the blockade of the activation of inflammatory, cell apoptosis-related signaling pathways. Quercetin may also serve as SARS-CoV-2 inhibitor by binding with the active sites of SARS-CoV-2 main protease 3CL and ACE2, therefore suppressing the functions of the proteins to cut the viral life cycle. In conclusion, Quercetin may be a novel therapeutic agent for COVID-19-induced AKI. Inhibition of inflammatory, cell apoptosis-related signaling pathways may be the critical mechanisms by which Quercetin protects kidney from SARS-CoV-2 injury.

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IL-17A and TNF-α as potential biomarkers for acute respiratory distress syndrome and mortality in patients with obesity and COVID-19

Cited by 49 publications

References 45 publications

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

COVID-19 severity in obese patients: Potential mechanisms and molecular targets for clinical intervention

Quercetin as a potential treatment for COVID-19-induced acute kidney injury: Based on network pharmacology and molecular docking study

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