A clinical and biological framework on the role of visceral fat tissue and leptin in SARS-CoV-2 infection related respiratory failure

Voort, Peter H. J. van der; Moser, Jill; Zandstra, D. F.; Kobold, Anneke C. Muller; Knoester, Marjolein; Calkhoven, Cornelis F.; Hamming, Inge; Meurs, Matijs van

doi:10.1101/2020.04.30.20086108

Cited by 3 publications

(3 citation statements)

References 29 publications

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“…However, the paper of van der Poort et al (2020) found that patients that have an increased Body Mass Index (BMI) also have increased leptin levels in serum, which they hypothesize could correlate with severity of the infection [ 195 , 196 ]. Interestingly, increased expression of the ACE2 receptor in the lung epithelia are positively correlated with obesity, indicating that obese individuals might be at higher risk for SARS-CoV-2 infection [ 195 , 196 ]. In conclusion, there is no robust evidence to either demonstrate or exclude that skin and adipose tissue harbor SARS-CoV-2 viral particles.…”

Section: Resultsmentioning

confidence: 99%

On the whereabouts of SARS-CoV-2 in the human body: A systematic review

et al. 2020

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Since SARS-CoV-2 appeared in the human population, the scientific community has scrambled to gather as much information as possible to find good strategies for the containment and treatment of this pandemic virus. Here, we performed a systematic review of the current (pre)published SARS-CoV-2 literature with a focus on the evidence concerning SARS-CoV-2 distribution in human tissues and viral shedding in body fluids. In addition, this evidence is aligned with published ACE2 entry-receptor (single cell) expression data across the human body to construct a viral distribution and ACE2 receptor body map. We highlight the broad organotropism of SARS-CoV-2, as many studies identified viral components (RNA, proteins) in multiple organs, including the pharynx, trachea, lungs, blood, heart, vessels, intestines, brain, male genitals and kidneys. This also implicates the presence of viral components in various body fluids such as mucus, saliva, urine, cerebrospinal fluid, semen and breast milk. The main SARS-CoV-2 entry receptor, ACE2, is expressed at different levels in multiple tissues throughout the human body, but its expression levels do not always correspond with SARS-CoV-2 detection, indicating that there is a complex interplay between virus and host. Together, these data shed new light on the current view of SARS-CoV-2 pathogenesis and lay the foundation for better diagnosis and treatment of COVID-19 patients.

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Section: Resultsmentioning

confidence: 99%

On the whereabouts of SARS-CoV-2 in the human body: A systematic review

et al. 2020

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“…In addition, high leptin levels have been associated with accumulation of alveolar fluid and increased inflammation upon hypoxia and ARDS [58]. Therefore, it may be hypothesised that excess visceral adipose tissue in patients with COVID-19 may drive disease progressionwhether or not affected by genderespecially through aggravating the cascade of hyperinflammatory reactions in the disease [59]. Ultimately, this 'cytokine storm' may lead to multiple organ failure in patients with COVID-19.…”

Section: Obesitymentioning

confidence: 99%

Angiotensin‐converting enzyme 2 (ACE2), SARS‐CoV‐2 and the pathophysiology of coronavirus disease 2019 (COVID‐19)

Bourgonje

Abdulle

Timens

et al. 2020

The Journal of Pathology

902

621

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Angiotensin‐converting enzyme 2 (ACE2) has been established as the functional host receptor for severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), the virus responsible for the current devastating worldwide pandemic of coronavirus disease 2019 (COVID‐19). ACE2 is abundantly expressed in a variety of cells residing in many different human organs. In human physiology, ACE2 is a pivotal counter‐regulatory enzyme to ACE by the breakdown of angiotensin II, the central player in the renin–angiotensin–aldosterone system (RAAS) and the main substrate of ACE2. Many factors have been associated with both altered ACE2 expression and COVID‐19 severity and progression, including age, sex, ethnicity, medication, and several co‐morbidities, such as cardiovascular disease and metabolic syndrome. Although ACE2 is widely distributed in various human tissues and many of its determinants have been well recognised, ACE2‐expressing organs do not equally participate in COVID‐19 pathophysiology, implying that other mechanisms are involved in orchestrating cellular infection resulting in tissue damage. Reports of pathologic findings in tissue specimens of COVID‐19 patients are rapidly emerging and confirm the established role of ACE2 expression and activity in disease pathogenesis. Identifying pathologic changes caused by SARS‐CoV‐2 infection is crucially important as it has major implications for understanding COVID‐19 pathophysiology and the development of evidence‐based treatment strategies. Currently, many interventional strategies are being explored in ongoing clinical trials, encompassing many drug classes and strategies, including antiviral drugs, biological response modifiers, and RAAS inhibitors. Ultimately, prevention is key to combat COVID‐19 and appropriate measures are being taken accordingly, including development of effective vaccines. In this review, we describe the role of ACE2 in COVID‐19 pathophysiology, including factors influencing ACE2 expression and activity in relation to COVID‐19 severity. In addition, we discuss the relevant pathological changes resulting from SARS‐CoV‐2 infection. Finally, we highlight a selection of potential treatment modalities for COVID‐19. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

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“…и др. Дисбаланс адипокинов и его роль в патогенезе новой коронавирусной тием дыхательной недостаточности, потребностью в ИВЛ и летальностью) была подтверждена целым рядом независимых исследований, проведенных в разных странах [31][32][33]. Метаанализ нескольких крупномасштабных эпидемиологических исследований свидетельствует о том, что с увеличением массы тела значительно возрастает и тяжесть заболевания [34][35][36].…”

Section: ожирение и нкиunclassified

Adipokine imbalance and its role in the pathogenesis of novel coronavirus infection

Bespalova,

Mitrichenko,

Kalyuzhin

et al. 2024

Bûll. sib. med.

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The review summarizes and analyzes the results of major foreign studies on the role of adipokine imbalance in the development of a severe course and complications of novel coronavirus infection (COVID-19). Adipokines are biologically active compounds produced by adipose tissue cells and involved in the regulation of metabolism and the functioning of the immune system. Obesity is a proven risk factor for severe COVID-19 due to high hormonal and metabolic activity of visceral adipose tissue. A deep understanding of COVID-19 pathogenesis from the point of view of the role of adipokine imbalance in it can provide the grounds for the development of effective pathogenetic approaches to the prevention of a severe course and complications of novel coronavirus infection.

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A clinical and biological framework on the role of visceral fat tissue and leptin in SARS-CoV-2 infection related respiratory failure

Cited by 3 publications

References 29 publications

On the whereabouts of SARS-CoV-2 in the human body: A systematic review

On the whereabouts of SARS-CoV-2 in the human body: A systematic review

Angiotensin‐converting enzyme 2 (ACE2), SARS‐CoV‐2 and the pathophysiology of coronavirus disease 2019 (COVID‐19)

Adipokine imbalance and its role in the pathogenesis of novel coronavirus infection

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