Key result
Activation of the renin-angiotensin-aldosterone system and elevated angiotensin II play a key role in oxidative stress, inflammation, and target organ damage in patients with type 2 diabetes.
This review summarizes the pathophysiological mechanisms by which angiotensin II and the broader renin-angiotensin-aldosterone system contribute to cardiovascular and renal disease in type 2 diabetes.
May reinforce RAAS inhibition in T2D; extends mechanistic understanding but leaves open targeted interventions.
Purpose of review Activation of the renin–angiotensin–aldosterone system and subsequent elevated levels of angiotensin II has been an area of intense focus in its relationship to oxidative stress, inflammation and target organ damage in patients with type 2 diabetes mellitus. Recent findings Exciting advances have been made in the past year in our understanding of extracellular matrix remodeling of perivascular tissue and diabetic nephropathy, particularly in regard to podocyte biology. In addition, the discovery of angiotensin-converting enzyme 2 and downstream angiotensin (1–7) has provided new insights into our understanding of how components of the renin–angiotensin–aldosterone system interact. Summary This review covers topical literature and attempts to provide insights into the clinical impact of these findings.
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Hayden et al. (2006) conducted a review in Type 2 diabetes mellitus with cardiovascular and renal disease. Angiotensin II was evaluated. Activation of the renin-angiotensin-aldosterone system and elevated angiotensin II play a key role in oxidative stress, inflammation, and target organ damage in patients with type 2 diabetes.
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