ReviewThe American journal of pathology2021
ACE2 Down-Regulation May Act as a Transient Molecular Disease Causing RAAS Dysregulation and Tissue Damage in the Microcirculatory Environment Among COVID-19 Patients.
Review in The American journal of pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
- Sildenafil for treating patients with COVID-19 and perfusion mismatch: a pilot randomized trial.Critical care (London, England) · 2022Trial
- Rationally Modified SARS-CoV-2 Spike Protein Impairs ACE2 Binding While Preserving Immunogenicity in Mice.Vaccines · 2026Article
- Renin-angiotensin imbalance promotes excessive fibrin deposition through M2 macrophage-derived tissue factor expression in eosinophilic chronic rhinosinusitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Vascular Immune Crosstalk in COVID-19: RAAS Biomarker Signature Linking Angiotensin II to Respiratory Compromise and Soluble ACE2 to IL-13 and FGF, Revealing Therapeutic Targets.International journal of molecular sciences · 2026Article
- The Role of Toll-like Receptors and Viral Infections in the Pathogenesis and Progression of Pulmonary Arterial Hypertension-A Narrative Review.International journal of molecular sciences · 2025Review
- Modulation of RAAS receptors and miRNAs in COVID-19: implications for disease severity, immune response, and potential therapeutic targets.BMC infectious diseases · 2025Observational
- COVID-19 and acute limb ischemia: latest hypotheses of pathophysiology and molecular mechanisms.Journal of Zhejiang University. Science. B · 2025Review
- COVID-19 vaccine-induced autoimmune hyperthyroidism: Graves' disease.Frontiers in immunology · 2025Review
- RAAS Overactivation and Mitochondrial Damage Signaling as Key Players in Lethal COVID-19.Current drug targets · 2025Article
- Food-Derived Up-Regulators and Activators of Angiotensin Converting Enzyme 2: A Review.Journal of agricultural and food chemistry · 2024Review
- Evaluation of blood pressure variation in recovered COVID-19 patients at one-year follow-up: a retrospective cohort study.BMC cardiovascular disorders · 2024Article
- The Role of Furin in the Pathogenesis of COVID-19-Associated Neurological Disorders.Life (Basel, Switzerland) · 2024Article
- Differential Ability of Spike Protein of SARS-CoV-2 Variants to Downregulate ACE2.International journal of molecular sciences · 2024Article
- Why have SGLT2 Inhibitors Failed to Achieve the Desired Success in COVID-19?Current pharmaceutical design · 2024Review
- Coronary microcirculatory dysfunction in hypercholesterolemic patients with COVID-19: potential benefit from cholesterol-lowering treatment.Annals of medicine · 2023Article
- Alveolar Hyperoxia and Exacerbation of Lung Injury in Critically Ill SARS-CoV-2 Pneumonia.Medical sciences (Basel, Switzerland) · 2023Review
- ACE2, ACE, DPPIV, PREP and CAT L enzymatic activities in COVID-19: imbalance of ACE2/ACE ratio and potential RAAS dysregulation in severe cases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Article
- ACE2 Receptor and TMPRSS2 Protein Expression Patterns in the Human Brainstem Reveal Anatomical Regions Potentially Vulnerable to SARS-CoV-2 Infection.ACS chemical neuroscience · 2023Article
- Graves' Disease after mRNA COVID-19 Vaccination, with the Presence of Autoimmune Antibodies Even One Year Later.Vaccines · 2023Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus 2, the etiologic agent of coronavirus disease 2019 (COVID-19) and the cause of the current pandemic, produces multiform manifestations throughout the body, causing indiscriminate damage to multiple organ systems, particularly the lungs, heart, brain, kidney, and vasculature. The aim of this review is to provide a new assessment of the data already available for COVID-19, exploring it as a transient molecular disease that causes negative regulation of angiotensin-converting enzyme 2, and consequently, deregulates the renin-angiotensin-aldosterone system, promoting important changes in the microcirculatory environment. Another goal of the article is to show how these microcirculatory changes may be responsible for the wide variety of injury mechanisms observed in different organs in this disease. The new concept of COVID-19 provides a unifying pathophysiological picture of this infection and offers fresh insights for a rational treatment strategy to combat this ongoing pandemic.
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