ArticleFrontiers in physiology2020
ACE2, COVID-19 Infection, Inflammation, and Coagulopathy: Missing Pieces in the Puzzle.
Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Gastrointestinal Sequelae of COVID-19: Investigating Post-Infection Complications-A Systematic Review.Viruses · 2024Pooled it
- The Role of ACE2 in SARS-CoV-2 Infection, Pathogenesis, and Antiviral Interventions.Journal of medical virology · 2025Review
- Lyophilized MSC-EVs attenuates COVID-19 pathogenesis by regulating the JAK/STAT pathway.Stem cell research & therapy · 2025Article
- Sex and other predictors of mortality in long-term follow-up of patients with cardiovascular disease and COVID-19: a single-center retrospective study.Scientific reports · 2025Article
- Attenuated cardiac autonomic function in patients with long-COVID with impaired orthostatic hemodynamics.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Article
- Article
- Interaction of SARS-CoV-2 and SARS-CoV-2 vaccines with renin angiotensin aldosterone system, clinical outcomes, and angiotensin (1-7) as a physiological treatment recommendation: hypothesis and theory article.Frontiers in medicine · 2025Article
- Angiotensin II-Real-Life Use and Literature Review.Medicina (Kaunas, Lithuania) · 2024Review
- Article
- Global Challenges After a Global Challenge: Lessons Learned from the COVID-19 Pandemic.Advances in experimental medicine and biology · 2024Article
- Female reproductive health during the COVID-19 pandemic: latest evidence and understanding.Archives of gynecology and obstetrics · 2023Review
- Sialylated Glycan Bindings from SARS-CoV-2 Spike Protein to Blood and Endothelial Cells Govern the Severe Morbidities of COVID-19.International journal of molecular sciences · 2023Review
- SARS-CoV-2 Impact on Red Blood Cell Morphology.Biomedicines · 2023Article
- Article
- Life-threatening bronchospasm induced by an angiotensin-converting enzyme inhibitor in a chronically ventilated patient: Diagnostic pitfalls and literature review.Respirology case reports · 2023Article
- Impact of Alteplase on Mortality in Critically Ill Patients with COVID-19 and Pulmonary Embolism.Viruses · 2023Article
- A U-shaped protection of altitude against mortality and infection of COVID-19 in Peru: an ecological study.BMC public health · 2023Article
- Higher proinflammatory responses possibly contributing to suppressed cytotoxicity in patients with COVID-19 associated mucormycosis.Immunobiology · 2023Article
- Vascular Aging and COVID-19.Angiology · 2023Review
- ACE2-Inhibitory Effects of Bromelain and Ficin in Colon Cancer Cells.Medicina (Kaunas, Lithuania) · 2023Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Engulfed by the grave consequences of the coronavirus disease 2019 (COVID-19) pandemic, a better understanding of the unique pattern of viral invasion and virulence is of utmost importance. Angiotensin (Ang)-converting enzyme (ACE) 2 is a key component in COVID-19 infection. Expressed on cell membranes in target pulmonary and intestinal host cells, ACE2 serves as an anchor for initial viral homing, binding to COVID-19 spike-protein domains to enable viral entry into cells and subsequent replication. Viral attachment is facilitated by a multiplicity of membranal and circulating proteases that further uncover attachment loci. Inherent or acquired enhancement of membrane ACE2 expression, likely leads to a higher degree of infection and may explain the predisposition to severe disease among males, diabetics, or patients with respiratory or cardiac diseases. Additionally, once attached, viral intracellular translocation and replication leads to depletion of membranal ACE2 through degradation and shedding. ACE2 generates Ang 1-7, which serves a critical role in counterbalancing the vasoconstrictive, pro-inflammatory, and pro-coagulant effects of ACE-induced Ang II. Therefore, Ang 1-7 may decline in tissues infected by COVID-19, leading to unopposed deleterious outcomes of Ang II. This likely leads to microcirculatory derangement with endothelial damage, profound inflammation, and coagulopathy that characterize the more severe clinical manifestations of COVID-19 infection. Our understanding of COVID-ACE2 associations is incomplete, and some conceptual formulations are currently speculative, leading to controversies over issues such as the usage of ACE inhibitors or Ang-receptor blockers (ARBs). This highlights the importance of focusing on ACE2 physiology in the evaluation and management of COVID-19 disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.