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. 2021 Feb 12;10(2):381. doi: 10.3390/cells10020381

Table 1.

Other organs/medical conditions and potential influence of renin-angiotensin system (RAS) on their function and/or occurrence.

Organs Data
Kidney •Exercise training attenuates the progression of glomerular sclerosis and renal interstitial fibrosis in chronic renal failure rats by increasing expression of RAS components such as angiotensinogen and angiotensin-converting enzyme (ACE) [164].
•Increase in AT2R expression after estrogen treatment in the mouse kidney [165].
•Estrogen treatment in OVX mice dramatically decreased the AT1R to AT2Rratio by upregulation of AT2R expression [165].
•Ang II actively participates in renal fibrosis and in the parts mediated by TGF- β [166].
•Irbesartan reduces the expression of TGF-β1 mRNA [166].
•In the rat kidney, the distribution of the AT4R was reported to occur in high levels in the proximal tubules [167].
•Infusion of Ang IV into the renal artery of rats resulted in increased renal cortical blood flow and urinary sodium excretion [168].
•AT2R mRNA has been reported to have a widespread distribution within the rat kidney [169].
Gallbladder •ACE2 suppressed tumor growth in gallbladder cancer [170].
•Lowered ACE2 expression was correlated with larger tumor size, high TNM stage, lymph node metastasis, and invasion in squamous cell/adenosquamous carcinoma patients [171].
Heart •Ang IV stimulated DNA and RNA synthesis in cultured rabbit cardiac fibroblast [172].
•The activation of ERK1/2 was critical for the growth-promoting actions of ang II in cardiac fibroblasts or prostate cancer cell subcultures [173].
•Enhanced vasoconstrictive effect of Ang II in AT2R-knockout mice [174].
•Vasodilatation due to AT2R overexpression in vascular smooth muscle cells [175].
•Ang IV stimulates protein synthesis in rabbit cardiac fibroblasts [172].
•Ang (1-7) treatment leads to decrease the ratio of expression of MMPs/TIMPs in human cardiocytes [176].
•Ang II induces SIF complex formation in neonatal rat cardiac myocytes in a time- and dose-dependent manner [177].
Muscle •Ang II stimulated angiogenesis in the rat cremaster muscle [178].
•Janus tyrosine kinase-STAT pathway directly through the AT1R in smooth muscle cells and cardiac myocytes [177].
•Cav-1 plays a critical role in the key signaling step in which angiotensin II induces the transactivation of the epidermal growth factor receptor (EGFR), leading to the hypertrophy and migration of vascular smooth muscle cells [179].
•Blockade of AT1R signaling reduced tumor growth, angiogenesis, and metastasis in the model of murine sarcoma and fibrosarcoma cells [180].
Stomach •The local production of Ang II in gastric cancer has been indicated to promote lymph node metastasis and cancer progression [180].
•Increased OS median in ACEI/ARB group compared to the non-ACEI /ARB group [181].
Testicles •Ang III and IV, and ACE2 may serve as the regulators of testicular steroidogenesis [182].
•Ang 1-7 can bind to a third receptor, specific to Ang 1-7 only (AT1-7/Mas receptor), which is also found in testes of fertile and infertile men [12].
•Main localization of Ang (1–7) and Mas receptor is observed in the Leydig cells [12].
•In non-obstructive azoospermia biopsies samples, Mas mRNA, protein, and ACE2 mRNA were lowered compared with biopsies from men with obstructive azoospermia [12].
Ovaries •Ang II increases the invasive potential of the highly-metastatic ovarian cancer cell line SKOV3 [183].
•RAS components like Ang (1-7) and Mas were localized to primordial, primary, secondary, and antral follicles, stroma, and corpora lutea of reproductive-age ovaries [21].
•High expression of AT1 predicted a shorter survival time for Grade 1 and Grade 2 ovary tumor patients [183].

RAS = Renin-angiotensin system, AT2 = angiotensin II, OVX = ovariectomized rat, TGF-β = transforming growth factor β1, AT4 = angiotensin IV, AT2R = angiotensin II receptor, TNM = Classification of Malignant Tumors, ERK1/2 = extracellular signaling-regulated kinase, MMPs/TIMPs = matrix metalloproteinases/tissue Inhibitor of metalloproteinase, SIF = Sis-inducing factor, AT1 = angiotensin I, OS = overall survival, ACEI/ARB = angiotensin-converting-enzyme inhibitors, ARB = angiotensin receptor blockers, ACE2 = angiotensin-converting enzyme 2.