Related Experiment Video
Updated: Feb 20, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
Published on: June 7, 2016
Angiotensin-converting enzyme 2 and renal disease
Vanessa R Williams1,2, James W Scholey1,2
1Institute of Medical Science, Faculty of Medicine, University of Toronto.
Angiotensin-converting enzyme 2 (ACE2) plays a protective role in kidney injury by regulating the renin-angiotensin system (RAS). Research explores ACE2
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Biochemistry
Background:
- The renin-angiotensin system (RAS) is crucial in cardiovascular and renal health.
- Angiotensin-converting enzyme 2 (ACE2) metabolizes angiotensin II to protective Ang-(1-7).
- ACE2 is abundant in the kidney and implicated in injury protection.
Purpose of the Study:
- To review current experimental and clinical findings on ACE2 in kidney injury.
- To examine the therapeutic potential of ACE2 in kidney disease treatment.
Main Methods:
- Review of experimental models investigating ACE2 induction.
- Analysis of clinical studies on ACE2 in diabetic kidney disease.
- Examination of ACE2's role in renal function, inflammation, and fibrosis.
Main Results:
- ACE2 upregulation in urine of diabetic patients suggests pathological shedding.
- Experimental models show ACE2 induction may improve renal function and reduce fibrosis.
- ACE2 is a critical regulator of angiotensin metabolism in renal disease pathogenesis.
Conclusions:
- ACE2 is a key regulator in the renin-angiotensin system and kidney disease.
- Human recombinant ACE2 offers a potential therapeutic strategy.
- Further research on ACE2's role will identify novel therapeutic targets for kidney disease.
Related Concept Videos
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
Antihypertensive Drugs: Direct Renin Inhibitors
Antihypertensive Drugs: Angiotensin II Receptor Blockers
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Hypertension II: Pathophysiology
Acute Kidney Injury II: Pathophysiology

