Expression of ACE and ACE2 in Individuals With Diabetic Kidney Disease and Healthy Controls

Loss of angiotensin-converting enzyme 2 enhances TGF-β/Smad-mediated renal fibrosis and NF-κB-driven renal inflammation in a mouse model of obstructive nephropathy

“…20 Similarly, in diabetic nephropathy, while upregulation of Ace2 is noted in the diabetic kidney in mice 8,10,21,22 and in humans, 23 downregulation of Aces is also reported. [24][25][26] The functional importance of Ace2 is now established by recent findings that loss of Ace2 promotes but administration of recombinant human ACE2 inhibits exogenous Ang II-induced hypertensive nephropathy and streptozotocin-induced diabetic nephropathy. [8][9][10][11]27 All these findings imply that Ace2 may protect against progressive renal injury in diseases associated with hypertension and diabetes.…”

“…This finding was consistent with the Ace2 protects renal fibrosis and inflammation Z Liu et al observation in both animals and patients with diabetes or IgA nephropathy. [21][22][23][24][25][26]28 Thus, Ace2 is an important counterregulator for systemic hypertension and locally in determining the disease progression by balancing the intrarenal Ang II generation and degradation pathways.…”

Decreased Expression of Angiotensin-Converting Enzyme 2 in Pancreatic Ductal Adenocarcinoma Is Associated with Tumor Progression

“…ACE2 has been shown to be a critical element in the conversion to hyperplasia via anti-apoptotic hormone [ANG II directly to ANG-(1-7)], which has the opposite function of ANG II (i.e., anti-proliferative and proapoptotic). ACE2 appears to counterbalance the ANG II-promoting effect of ACE, and plays a protective role in many diseases (Raizada and Ferreira 2007;Mizuiri et al 2008;Wang et al 2008). However, the expression and role of ACE2 in PDAC are still unclear.…”

The angiotensin-converting enzyme 2 in tumor growth and tumor-associated angiogenesis in non-small cell lung cancer

“…Imai et al (28) found tumor size and VEGFa reduced significantly in AT1a -/-mice treated with TCV-116 (an AT1 receptor antagonist) compared with untreated mice. As a recently reported homologue of ACE, ACE2 is a new component of the updated RAS shown to be critical in the balance between AngII and Ang-(1-7) and to play a protective role in many diseases (29)(30)(31). However, its expression and effect in NSCLC remain unclear.…”