Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.24.B1 (
angiotensin-converting enzyme 2
)
1,025
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The degradation of ANG II by
angiotensin-converting enzyme 2
(
ACE2
), leading to the formation of ANG(1-7), is an important step in the regulation of the renin-angiotensin-aldosterone system (RAAS), and one that is significantly altered in the diabetic kidney. This study examined the role of
ACE2
in the hyperfiltration associated with diabetes. Streptozotocin diabetes was induced in male C57BL6 mice and
ACE2
knockout (KO) mice. C57BL6 mice were further randomized to receive the selective
ACE2
inhibitor MLN-4760. After 2 wk of study, animals were subjected to micropuncture experiments. The renal reserve was further assessed in C57BL6 mice and
ACE2
KO mice after exposure to a high-protein diet. The induction of diabetes in wild-type mice was associated with increased renal
ACE2
activity, hyperfiltration, and renal hypertrophy. On micropuncture, diabetes was associated with increased tubular free flow and stop-flow pressure, enhanced tubuloglomerular feedback reactivity, and an increased maximal response indicative of increased glomerular hydrostatic capillary pressure. Each of these increases were prevented in diabetic
ACE2
KO mice and diabetic mice treated with a selective
ACE2
inhibitor for 2 wk. However, unlike chronically treated animals,
ACE2
inhibition with MLN-4760 had no acute effect on stop-flow pressure or tubuloglomerular feedback reactivity.
ACE2
KO mice also failed to increase their
creatinine
clearance in response to a high-protein diet. The results of our study suggest that
ACE2
plays a key role in the recruitment of the renal reserve and hyperfiltration associated with diabetes.
...
PMID:Angiotensin-converting enzyme 2 mediates hyperfiltration associated with diabetes. 2447 84
Cyclosporine, an immunosuppressive drug, exhibits a toxic effect on renal and vascular systems. The present study investigated whether resveratrol treatment alleviates renal and vascular injury induced by cyclosporine. Cyclosporine (25 mg/kg per day, s.c.) was given for 7 days to rats either alone or in combination with resveratrol (10 mg/kg per day, i.p.). Relaxation and contraction responses of aorta were examined. Serum levels of blood urea nitrogen,
creatinine
, angiotensin II, and angiotensin 1-7 were measured. Histopathological examinations as well as immunostaining for 4-hydroxynonenal and nitrotyrosine were performed in the kidney. RNA expressions of renin-angiotensin system components were also measured in renal and aortic tissues. Cyclosporine decreased the endothelium-dependent relaxation and increased vascular contraction in the aorta. It caused renal tubular degeneration and increased immunostaining for 4-hydroxynonenal, an oxidative stress marker. Cyclosporine also caused upregulations of the vasoconstrictive renin-angiotensin system components in renal (angiotensin-converting enzyme) and aortic (angiotensin II type 1 receptor) tissues. Resveratrol co-treatment prevented the cyclosporine-related deteriorations. Moreover, it induced the expressions of vasodilatory effective
angiotensin-converting enzyme 2
and angiotensin II type 2 receptor in aorta and kidney, respectively. We conclude that resveratrol may be effective in preventing cyclosporine-induced renal tubular degeneration and vascular dysfunction at least in part by modulating the renin-angiotensin system.
...
PMID:Resveratrol ameliorates the cyclosporine-induced vascular and renal impairments: possible impact of the modulation of renin-angiotensin system. 3161 43
COVID-19 has become a pandemic and it has already spread to at least 171 countries/regions. Chronic kidney disease (CKD) is a global public health problem with a total of approximately 850 million patients with CKD worldwide and 119.5 million in China. Severe COVID-19 infection may damage the kidney and cause acute tubular necrosis, leading to proteinuria, hematuria and elevated serum
creatinine
. Since the SARS-CoV-2 enters the cells by binding to the
angiotensin-converting enzyme 2
receptor, some doctors question its ability to increase the risk and severity of developing COVID-19. Neither clinical data nor basic scientific evidence supports this assumption. Therefore, patients who take angiotensin-converting enzyme inhibitor or angiotensin receptor blocker are not advised to change their therapy. Patients with CKD are generally the elderly population suffering from multiple comorbidities. Moreover, some patients with CKD might need to take glucocorticoids and immunosuppressants. Dialysis patients are recurrently exposed to a possible contaminated environment because their routine treatment usually requires three dialysis sessions per week. Considering all the above reasons, patients with CKD are more vulnerable to COVID-19 than the general population. The development of COVID-19 may worsen the impaired kidney function and further lead to rapid deterioration of kidney function and even death. Strict comprehensive protocols should be followed to prevent the spread of COVID-19 among patients with CKD. In this review, we provide some practical management recommendations for health care providers, patients with CKD, dialysis patients and dialysis facilities.
...
PMID:Management recommendations for patients with chronic kidney disease during the novel coronavirus disease 2019 (COVID-19) epidemic. 3240 37
There are several risk factors for worse outcomes in patients with coronavirus 2019 disease (COVID-19). Patients with hypertension appear to have a poor prognosis, but there is no direct evidence that hypertension increases the risk of new infection or adverse outcomes independent of age and other risk factors. There is also concern about use of renin-angiotensin system (RAS) inhibitors due to a key role of
angiotensin-converting enzyme 2
receptors in the entry of the SARS-CoV-2 virus into cells. However, there is little evidence that use of RAS inhibitors increases the risk of SARS-CoV-2 virus infection or worsens the course of COVID-19. Therefore, antihypertensive therapy with these agents should be continued. In addition to acute respiratory distress syndrome, patients with severe COVID-19 can develop myocardial injury and cytokine storm, resulting in heart failure, arteriovenous thrombosis, and kidney injury. Troponin, N-terminal pro-B-type natriuretic peptide, D-dimer, and serum
creatinine
are biomarkers for these complications and can be used to monitor patients with COVID-19 and for risk stratification. Other factors that need to be incorporated into patient management strategies during the pandemic include regular exercise to maintain good health status and monitoring of psychological well-being. For the ongoing management of patients with hypertension, telemedicine-based home blood pressure monitoring strategies can facilitate maintenance of good blood pressure control while social distancing is maintained. Overall, multidisciplinary management of COVID-19 based on a rapidly growing body of evidence will help ensure the best possible outcomes for patients, including those with risk factors such as hypertension.
...
PMID:COVID-19 and hypertension-evidence and practical management: Guidance from the HOPE Asia Network. 3264 74