What is the clinical evidence from this study?

Study design: Review. Population: SARS-CoV-2 infection. Intervention: SARS-CoV-2 infection.

What question did this study set out to answer?

To describe the mechanism by which SARS-CoV-2 binding to ACE2 disrupts the renin-angiotensin-aldosterone system and to evaluate its clinical impact on lung injury.

April 26, 2021International Journal of Molecular SciencesOpen Access

SARS-CoV-2 binding to ACE2 reduces its cell surface activity, leading to an atherogenic imbalance between angiotensin 2 and angiotensin (1-7) that may increase lung damage.

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Population

Patients infected with SARS-CoV-2

Design

Review

Key result

SARS-CoV-2 binding to ACE2 reduces its cell surface activity, leading to an atherogenic imbalance between angiotensin 2 and angiotensin (1-7) that may increase lung damage.

Authors

ADAgnieszka Dettlaff‐PokoraGdańsk Medical University JŚJulian ŚwierczyńskiKoszalin University of Technology

Discussion

Member takes

Overview

Suggests RAAS imbalance contributes to COVID-19 lung injury; leaves open whether targeting ACE2 degradation improves outcomes.

Key Points

To describe the mechanism by which SARS-CoV-2 binding to ACE2 disrupts the renin-angiotensin-aldosterone system and to evaluate its clinical impact on lung injury.
Mechanistic synthesis of ACE2 enzymatic pathways involving the conversion of angiotensin 2 to angiotensin (1-7) and angiotensin (1-9) synthesis.
Evaluation of viral entry dynamics, cellular internalization, and downstream degradation of membrane-bound ACE2 during infection.
SARS-CoV-2 binding triggers the internalization and degradation of cell-surface ACE2, markedly diminishing its enzymatic activity.
Loss of functional ACE2 reduces protective, vasodilating angiotensin (1-7) while increasing vasoconstrictive, atherogenic angiotensin 2, driving pulmonary tissue damage.

Structured PICO

Population

Patients infected with SARS-CoV-2

SARS-CoV-2 infection disrupts the RAAS balance by downregulating ACE2, potentially exacerbating lung injury through increased angiotensin 2 levels.

Cite This Study

Dettlaff‐Pokora et al. (2021) conducted a review in SARS-CoV-2 infection. SARS-CoV-2 infection was evaluated. SARS-CoV-2 binding to ACE2 reduces its cell surface activity, leading to an atherogenic imbalance between angiotensin 2 and angiotensin (1-7) that may increase lung damage.

synapsesocial.com/papers/6a98bc79b0871bb756e10768 https://doi.org/10.3390/ijms22094503

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April 26, 2021International Journal of Molecular SciencesOpen Access

SARS-CoV-2 binding to ACE2 reduces its cell surface activity, leading to an atherogenic imbalance between angiotensin 2 and angiotensin (1-7) that may increase lung damage.

View Full Paper

Ask AI

Bookmark

Population

Patients infected with SARS-CoV-2

Design

Review

Key result

SARS-CoV-2 binding to ACE2 reduces its cell surface activity, leading to an atherogenic imbalance between angiotensin 2 and angiotensin (1-7) that may increase lung damage.

Authors

ADAgnieszka Dettlaff‐PokoraGdańsk Medical University JŚJulian ŚwierczyńskiKoszalin University of Technology

Discussion

Member takes

Overview

Suggests RAAS imbalance contributes to COVID-19 lung injury; leaves open whether targeting ACE2 degradation improves outcomes.

Key Points

To describe the mechanism by which SARS-CoV-2 binding to ACE2 disrupts the renin-angiotensin-aldosterone system and to evaluate its clinical impact on lung injury.
Mechanistic synthesis of ACE2 enzymatic pathways involving the conversion of angiotensin 2 to angiotensin (1-7) and angiotensin (1-9) synthesis.
Evaluation of viral entry dynamics, cellular internalization, and downstream degradation of membrane-bound ACE2 during infection.
SARS-CoV-2 binding triggers the internalization and degradation of cell-surface ACE2, markedly diminishing its enzymatic activity.
Loss of functional ACE2 reduces protective, vasodilating angiotensin (1-7) while increasing vasoconstrictive, atherogenic angiotensin 2, driving pulmonary tissue damage.

Structured PICO

Population

Patients infected with SARS-CoV-2

SARS-CoV-2 infection disrupts the RAAS balance by downregulating ACE2, potentially exacerbating lung injury through increased angiotensin 2 levels.

Cite This Study

synapsesocial.com/papers/6a98bc79b0871bb756e10768 https://doi.org/10.3390/ijms22094503

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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