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This article was the subject of a Wiki Education Foundation-supported course assignment, between 3 September 2020 and 14 December 2020. Further details are available on the course page. Student editor(s): Dinahcann.
Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT ( talk) 14:17, 16 January 2022 (UTC)
Can anybody actually find that statement in reference 23? — Preceding unsigned comment added by 96.242.2.70 ( talk) 23:20, 17 March 2020 (UTC)
Good point. I read the article twice but cannot find any such comment. This short paragraph is a paraphrase of a recent letter to the editor in Lancet, with the same references. I searched PubMed but did not find any clear evidence to support the statement. Valmataro ( talk) 14:58, 18 March 2020 (UTC)
Thank you for the review but it also does not support the author claim from the Lancet article. I finally found this article describing that ACE inhibition does upregulate cardiac ACE2 mRNA expression in rats: Ferrario et al. 2005. — Preceding unsigned comment added by 96.242.2.70 ( talk) 20:41, 23 March 2020 (UTC)
Recent additions to this article indirectly claim that there is a difference between "ACE2" and "ACE2 receptor". I very much doubt this is the case. All the literature I have read on related subjects treat those terms interchangeably and/or describe them in the same terms.-- Dpratt71 ( talk) 16:52, 17 March 2020 (UTC)
"ACE2 receptor" makes no sense. ACE2 is ITSELF the receptor for SARS-CoV and SARS-CoV-2 on respiratory tract cells. In normal function, ACE2 = angiotensin converting enzyme 2 "catalyses the conversion of angiotensin I to the nonapeptide angiotensin[1–9][5] or the conversion of angiotensin II to angiotensin 1–7.[6][7]". -- Canavalia ( talk) 19:29, 17 March 2020 (UTC)
That was my understanding, thank you for confirming, Canavalia. To further clarify, I think the term "ACE2 receptor" makes sense, it's just a bit redundant. The "ACE2 receptor" is not a receptor for ACE2, ACE2 is the receptor, as you say. As such, I believe this statement in the article is in error and should be removed (along with any corresponding edits):
This might lead some to suggest that decreasing the levels of ACE2, in cells, might help in fighting the infection, but that conflates ACE2 with the ACE2 receptor.
I'd vastly prefer someone with more subject knowledge make that edit (or at least someone with more WP editing knowledge), but I may get up the nerve to do it otherwise. -- Dpratt71 ( talk) 18:15, 17 March 2020 (UTC)
Reply It seems like they're the same according to the reference provided that they're reliable. [1] [2] [3] [4] For instance, ACE inhibitor is literally Angiotensin-converting enzyme inhibitor. [5]
There are some enzyme binding sites, alias receptor, on every enzyme though I am not confident in my answer. [6]
References
In cell lines, angiotensin-converting enzyme 2 (ACE2) has been identified as a potential SARS-CoV receptor.
Our results suggest an important role of ACE inhibitors, but not ARBs, in reducing the risk of pneumonia. These data may discourage the withdrawal of ACE inhibitors in some patients with tolerable adverse events (namely, cough) who are at particularly high risk of pneumonia. ACE inhibitors also lowered the risk of pneumonia related mortality, mainly in patients with established disease, but the robustness of the evidence was weaker.
Mechanisms of Action: ACE inhibitors act by inhibiting one of several proteases responsible for cleaving the decapeptide Ang I to form the octapeptide Ang II. Because ACE is also the enzyme that degrades bradykinin, ACE inhibitors increase circulating and tissue levels of bradykinin (Fig. 8.4).
Non-steroidal anti-inflammatory drugs (NSAIDs) are the competitive inhibitors of cyclooxygenase (COX), the enzyme which mediates the bioconversion of arachidonic acid to inflammatory prostaglandins (PGs).
Angiotensin-converting enzyme inhibitors: ACE inhibitors have been demonstrated to reduce sudden cardiac death in some studies of persons with CHF.24,56
ACE inhibitors are classified according to the chemical structure of the site of binding (sulfhydryl, phosphinyl, carboxyl) to the active center of ACE.
@ Seppi333: May I have your opinion on this? Thank you!
-- Reciprocater ( talk) —Preceding undated comment added 14:42, 20 March 2020 (UTC)
Reply ACE2 is the enzyme, while there is a surface protein on some cells that allows entry of ACE2 into the cell, the "receptor". They are very different things. Cells have receptors to allow entry of ACE2 for evolutionary biological processes. Certain viruses can and do co-opt that entry mechanism to gain entry to the cell. I don't have references to hand, this is what I have learned through listening to TWiV. Pete Miller.
The role of ACE2 in SARS-CoV and SARS-CoV-2 is complicated. The following about ACE in SARS (which should also apply equally to SARS-CoV-2) is clearest explanation I have been able to find:
There are a number of things going on here:
This has immediate implications for the continued use of blood pressure lower ACE inhibitors and ABRs in the environment of the coronavirus pandemic. The current recommendation is not to change standard prescribing practice. Boghog ( talk) 06:15, 21 March 2020 (UTC)
Dear many authors of this page (
Boghog,
Valmataro,
Reciprocater,
John B123), I would like to please request, given the large number of page views that is received, that edits strive to make the content as understandable to the lay and non biomedically-trained reader as possible. This is the lead at the moment:
Angiotensin converting enzyme 2 (ACE2, Angiotensin I converting enzyme 2)[5] is an enzyme expressed on the membrane of many cell types, including epithelial cells of the pulmonary alveolus and small intestine enterocytes.[6] It is an exopeptidase that catalyses the cleavage of angiotensin I into the nonapeptide angiotensin 1-9, and angiotensin II into angiotensin 1–7, which acts as a vasodilator.[7][8][9] ACE2 is a single-pass type I membrane protein.[10] It is also shed from cells and released into the blood stream and ultimately urine, by proteolytic cleavage.[11][12] The membrane-bound form of ACE2 serves as the entry point into human cells for some human coronaviruses.
This is not understandable to lay editors!! Here are some examples of some methods things can be changed:
Could editors please take readers into account when editing? It is possible to be both accurate and easy to read. Being "scientific" doesn't mean that it has to be incomprehensible; but the current state leaves the article only understandable to people with university level training, which is not ideal. Cheers -- Tom (LT) ( talk) 23:18, 21 March 2020 (UTC)
in terms of whatin your addition of {{ what}} in Angiotensin-converting_enzyme_2#Human_recombinant_ACE2_(rhACE2)? I don't fully understand you. English is my second language. Thank you. -- Reciprocater (Talk) 07:35, 30 March 2020 (UTC)
References
The interaction of the spike protein of the coronavirus with ACE2 induces a drop in the levels of ACE2 in cells through internalization and degradation of the protein and hence may contribute to lung damage.[18]
is a comparative study as opposed to a review article IMO.
is a comment rather than a review article either.
Both ACE inhibitors and angiotensin receptor blockers (ARBs) that are used to treat high blood pressure have been shown to upregulate ACE2 expression hence may affect the severity of coronavirus infections.
is not supported by any reference.
What the systematic review and meta-analysis for human says?
Use of ACE inhibitors was associated with a significant 34% reduction in risk of pneumonia compared with controls (odds ratio 0.66, 95% confidence interval 0.55 to 0.80; I2=79%). The NNT for 2.0 years was 65 (48 to 112). The magnitude of the risk reduction was similar across all study designs (P=0.78 for subgroup differences). Treatment with ACE inhibitors was associated with a significant 27% reduction in risk of pneumonia related mortality compared with controls (0.73, 0.58 to 0.92; I2=51%), without significant differences between estimates from randomised controlled trials and observational studies (P=0.76). In this systematic review we found that treatment with angiotensin converting enzyme (ACE) inhibitors was associated with a significant reduction in risk of pneumonia compared with control treatment and angiotensin receptor blockers (ARBs); the magnitude of this reduction (about one third) was similar across studies with different designs (randomised controlled trials, cohort, and case-control studies). The risk of pneumonia was also reduced in patients treated with ACE inhibitors who were at higher risk of pneumonia, in particular those with stroke and heart failure. Use of ACE inhibitors was also associated with a reduction in pneumonia related mortality, although the results were less robust than for overall risk of pneumonia; it is uncertain if differences exist between ACE inhibitors and ARBs for this outcome.
Taken together, I politely ask folks to review the statements quoted from the body of Angiotensin-converting_enzyme_2 shown above. Thank you!
-- Reciprocater ( talk) 07:08, 22 March 2020 (UTC)
Italy (finally..) published some epidemiological data [1], English [2] : "Before admission to hospital 27% resp 16% of the later deceased were taking ACE inhibitors resp. Sartans". Did not see any further analysis of this yet but given the age (avg 78) of the dead and prescription practice in Europe I don't see any dramatic effect upon first glance. Arterial hypertension had a prevalence of some 72% in this population so if anything there is a hint of a protective effect. Some Italian prescription data [3]. Richiez ( talk) 18:59, 3 April 2020 (UTC)
Some data from Germany [4] Richiez ( talk) 18:36, 4 April 2020 (UTC)
Guang Yang et al, "Angiotensin II Receptor Blockers and Angiotensin-Converting Enzyme Inhibitors Usage is Associated with Improved Inflammatory Status and Clinical Outcomes in COVID-19 Patients With Hypertension" [5]
Yingxia Liu et al, "Anti-hypertensive Angiotensin II receptor blockers associated to mitigation of disease severity in elderly COVID-19 patients" [6] - of interest this also has some data on beta blockers, thiazides and calcium channel blockers. Although they didn't collect enough patients to get statistically significant data on thiazides, ACEIs, BBs and CCBs there are trends for thiazides (which appear safe or beneficial) and CCBs. Richiez ( talk) 20:07, 10 April 2020 (UTC)
Does Angiotensin II “AT-II” bind with ACE2 at a site similar to where the Covid spike protein binds?
If so, are there epitopes on AT-II that are antigenically similar to epitopes on the COVID spike protein?
Why might this matter?
Because if so, potentially could
Cross React with AT-II, effectively Competing with ACE2 for AT-II (and potentially dysregulating the breakdown of AT-II with widespread downstream physiological/ pathological impact) ?
Any info on this?
Thanks.
G. Holt 2600:1002:B02F:522D:243F:79D8:86DA:7150 ( talk) 19:36, 29 November 2021 (UTC)
Please see previous question 2600:1002:B02F:522D:243F:79D8:86DA:7150 ( talk) 19:40, 29 November 2021 (UTC)
Possible dysregulation of RAAS? 2600:1002:B02A:E229:A0E8:E61B:27BD:B365 ( talk) 21:24, 7 December 2021 (UTC)
According to Oudit et al (2023): SARS-CoV-2’s viral tropism is dependent on ACE2 tissue distribution and expression. I am not sure if this fact is already included in the article, because it is too technical for me. If it is missing, I ask that we include it. Forich ( talk) 03:08, 9 March 2023 (UTC)
This article is rated C-class on Wikipedia's
content assessment scale. It is of interest to the following WikiProjects: | ||||||||||||||||||||||||||||||||||
|
Ideal sources for Wikipedia's health content are defined in the guideline
Wikipedia:Identifying reliable sources (medicine) and are typically
review articles. Here are links to possibly useful sources of information about Angiotensin-converting enzyme 2.
|
Daily pageviews of this article
A graph should have been displayed here but
graphs are temporarily disabled. Until they are enabled again, visit the interactive graph at
pageviews.wmcloud.org |
This article was the subject of a Wiki Education Foundation-supported course assignment, between 3 September 2020 and 14 December 2020. Further details are available on the course page. Student editor(s): Dinahcann.
Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT ( talk) 14:17, 16 January 2022 (UTC)
Can anybody actually find that statement in reference 23? — Preceding unsigned comment added by 96.242.2.70 ( talk) 23:20, 17 March 2020 (UTC)
Good point. I read the article twice but cannot find any such comment. This short paragraph is a paraphrase of a recent letter to the editor in Lancet, with the same references. I searched PubMed but did not find any clear evidence to support the statement. Valmataro ( talk) 14:58, 18 March 2020 (UTC)
Thank you for the review but it also does not support the author claim from the Lancet article. I finally found this article describing that ACE inhibition does upregulate cardiac ACE2 mRNA expression in rats: Ferrario et al. 2005. — Preceding unsigned comment added by 96.242.2.70 ( talk) 20:41, 23 March 2020 (UTC)
Recent additions to this article indirectly claim that there is a difference between "ACE2" and "ACE2 receptor". I very much doubt this is the case. All the literature I have read on related subjects treat those terms interchangeably and/or describe them in the same terms.-- Dpratt71 ( talk) 16:52, 17 March 2020 (UTC)
"ACE2 receptor" makes no sense. ACE2 is ITSELF the receptor for SARS-CoV and SARS-CoV-2 on respiratory tract cells. In normal function, ACE2 = angiotensin converting enzyme 2 "catalyses the conversion of angiotensin I to the nonapeptide angiotensin[1–9][5] or the conversion of angiotensin II to angiotensin 1–7.[6][7]". -- Canavalia ( talk) 19:29, 17 March 2020 (UTC)
That was my understanding, thank you for confirming, Canavalia. To further clarify, I think the term "ACE2 receptor" makes sense, it's just a bit redundant. The "ACE2 receptor" is not a receptor for ACE2, ACE2 is the receptor, as you say. As such, I believe this statement in the article is in error and should be removed (along with any corresponding edits):
This might lead some to suggest that decreasing the levels of ACE2, in cells, might help in fighting the infection, but that conflates ACE2 with the ACE2 receptor.
I'd vastly prefer someone with more subject knowledge make that edit (or at least someone with more WP editing knowledge), but I may get up the nerve to do it otherwise. -- Dpratt71 ( talk) 18:15, 17 March 2020 (UTC)
Reply It seems like they're the same according to the reference provided that they're reliable. [1] [2] [3] [4] For instance, ACE inhibitor is literally Angiotensin-converting enzyme inhibitor. [5]
There are some enzyme binding sites, alias receptor, on every enzyme though I am not confident in my answer. [6]
References
In cell lines, angiotensin-converting enzyme 2 (ACE2) has been identified as a potential SARS-CoV receptor.
Our results suggest an important role of ACE inhibitors, but not ARBs, in reducing the risk of pneumonia. These data may discourage the withdrawal of ACE inhibitors in some patients with tolerable adverse events (namely, cough) who are at particularly high risk of pneumonia. ACE inhibitors also lowered the risk of pneumonia related mortality, mainly in patients with established disease, but the robustness of the evidence was weaker.
Mechanisms of Action: ACE inhibitors act by inhibiting one of several proteases responsible for cleaving the decapeptide Ang I to form the octapeptide Ang II. Because ACE is also the enzyme that degrades bradykinin, ACE inhibitors increase circulating and tissue levels of bradykinin (Fig. 8.4).
Non-steroidal anti-inflammatory drugs (NSAIDs) are the competitive inhibitors of cyclooxygenase (COX), the enzyme which mediates the bioconversion of arachidonic acid to inflammatory prostaglandins (PGs).
Angiotensin-converting enzyme inhibitors: ACE inhibitors have been demonstrated to reduce sudden cardiac death in some studies of persons with CHF.24,56
ACE inhibitors are classified according to the chemical structure of the site of binding (sulfhydryl, phosphinyl, carboxyl) to the active center of ACE.
@ Seppi333: May I have your opinion on this? Thank you!
-- Reciprocater ( talk) —Preceding undated comment added 14:42, 20 March 2020 (UTC)
Reply ACE2 is the enzyme, while there is a surface protein on some cells that allows entry of ACE2 into the cell, the "receptor". They are very different things. Cells have receptors to allow entry of ACE2 for evolutionary biological processes. Certain viruses can and do co-opt that entry mechanism to gain entry to the cell. I don't have references to hand, this is what I have learned through listening to TWiV. Pete Miller.
The role of ACE2 in SARS-CoV and SARS-CoV-2 is complicated. The following about ACE in SARS (which should also apply equally to SARS-CoV-2) is clearest explanation I have been able to find:
There are a number of things going on here:
This has immediate implications for the continued use of blood pressure lower ACE inhibitors and ABRs in the environment of the coronavirus pandemic. The current recommendation is not to change standard prescribing practice. Boghog ( talk) 06:15, 21 March 2020 (UTC)
Dear many authors of this page (
Boghog,
Valmataro,
Reciprocater,
John B123), I would like to please request, given the large number of page views that is received, that edits strive to make the content as understandable to the lay and non biomedically-trained reader as possible. This is the lead at the moment:
Angiotensin converting enzyme 2 (ACE2, Angiotensin I converting enzyme 2)[5] is an enzyme expressed on the membrane of many cell types, including epithelial cells of the pulmonary alveolus and small intestine enterocytes.[6] It is an exopeptidase that catalyses the cleavage of angiotensin I into the nonapeptide angiotensin 1-9, and angiotensin II into angiotensin 1–7, which acts as a vasodilator.[7][8][9] ACE2 is a single-pass type I membrane protein.[10] It is also shed from cells and released into the blood stream and ultimately urine, by proteolytic cleavage.[11][12] The membrane-bound form of ACE2 serves as the entry point into human cells for some human coronaviruses.
This is not understandable to lay editors!! Here are some examples of some methods things can be changed:
Could editors please take readers into account when editing? It is possible to be both accurate and easy to read. Being "scientific" doesn't mean that it has to be incomprehensible; but the current state leaves the article only understandable to people with university level training, which is not ideal. Cheers -- Tom (LT) ( talk) 23:18, 21 March 2020 (UTC)
in terms of whatin your addition of {{ what}} in Angiotensin-converting_enzyme_2#Human_recombinant_ACE2_(rhACE2)? I don't fully understand you. English is my second language. Thank you. -- Reciprocater (Talk) 07:35, 30 March 2020 (UTC)
References
The interaction of the spike protein of the coronavirus with ACE2 induces a drop in the levels of ACE2 in cells through internalization and degradation of the protein and hence may contribute to lung damage.[18]
is a comparative study as opposed to a review article IMO.
is a comment rather than a review article either.
Both ACE inhibitors and angiotensin receptor blockers (ARBs) that are used to treat high blood pressure have been shown to upregulate ACE2 expression hence may affect the severity of coronavirus infections.
is not supported by any reference.
What the systematic review and meta-analysis for human says?
Use of ACE inhibitors was associated with a significant 34% reduction in risk of pneumonia compared with controls (odds ratio 0.66, 95% confidence interval 0.55 to 0.80; I2=79%). The NNT for 2.0 years was 65 (48 to 112). The magnitude of the risk reduction was similar across all study designs (P=0.78 for subgroup differences). Treatment with ACE inhibitors was associated with a significant 27% reduction in risk of pneumonia related mortality compared with controls (0.73, 0.58 to 0.92; I2=51%), without significant differences between estimates from randomised controlled trials and observational studies (P=0.76). In this systematic review we found that treatment with angiotensin converting enzyme (ACE) inhibitors was associated with a significant reduction in risk of pneumonia compared with control treatment and angiotensin receptor blockers (ARBs); the magnitude of this reduction (about one third) was similar across studies with different designs (randomised controlled trials, cohort, and case-control studies). The risk of pneumonia was also reduced in patients treated with ACE inhibitors who were at higher risk of pneumonia, in particular those with stroke and heart failure. Use of ACE inhibitors was also associated with a reduction in pneumonia related mortality, although the results were less robust than for overall risk of pneumonia; it is uncertain if differences exist between ACE inhibitors and ARBs for this outcome.
Taken together, I politely ask folks to review the statements quoted from the body of Angiotensin-converting_enzyme_2 shown above. Thank you!
-- Reciprocater ( talk) 07:08, 22 March 2020 (UTC)
Italy (finally..) published some epidemiological data [1], English [2] : "Before admission to hospital 27% resp 16% of the later deceased were taking ACE inhibitors resp. Sartans". Did not see any further analysis of this yet but given the age (avg 78) of the dead and prescription practice in Europe I don't see any dramatic effect upon first glance. Arterial hypertension had a prevalence of some 72% in this population so if anything there is a hint of a protective effect. Some Italian prescription data [3]. Richiez ( talk) 18:59, 3 April 2020 (UTC)
Some data from Germany [4] Richiez ( talk) 18:36, 4 April 2020 (UTC)
Guang Yang et al, "Angiotensin II Receptor Blockers and Angiotensin-Converting Enzyme Inhibitors Usage is Associated with Improved Inflammatory Status and Clinical Outcomes in COVID-19 Patients With Hypertension" [5]
Yingxia Liu et al, "Anti-hypertensive Angiotensin II receptor blockers associated to mitigation of disease severity in elderly COVID-19 patients" [6] - of interest this also has some data on beta blockers, thiazides and calcium channel blockers. Although they didn't collect enough patients to get statistically significant data on thiazides, ACEIs, BBs and CCBs there are trends for thiazides (which appear safe or beneficial) and CCBs. Richiez ( talk) 20:07, 10 April 2020 (UTC)
Does Angiotensin II “AT-II” bind with ACE2 at a site similar to where the Covid spike protein binds?
If so, are there epitopes on AT-II that are antigenically similar to epitopes on the COVID spike protein?
Why might this matter?
Because if so, potentially could
Cross React with AT-II, effectively Competing with ACE2 for AT-II (and potentially dysregulating the breakdown of AT-II with widespread downstream physiological/ pathological impact) ?
Any info on this?
Thanks.
G. Holt 2600:1002:B02F:522D:243F:79D8:86DA:7150 ( talk) 19:36, 29 November 2021 (UTC)
Please see previous question 2600:1002:B02F:522D:243F:79D8:86DA:7150 ( talk) 19:40, 29 November 2021 (UTC)
Possible dysregulation of RAAS? 2600:1002:B02A:E229:A0E8:E61B:27BD:B365 ( talk) 21:24, 7 December 2021 (UTC)
According to Oudit et al (2023): SARS-CoV-2’s viral tropism is dependent on ACE2 tissue distribution and expression. I am not sure if this fact is already included in the article, because it is too technical for me. If it is missing, I ask that we include it. Forich ( talk) 03:08, 9 March 2023 (UTC)