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Drp1 fission11/6/2023 ![]() Ocaranza MP, Moya J, Barrientos V, Alzamora R, Hevia D, Morales C, Pinto M, Escudero N, García L, Novoa U, Ayala P, Díaz-Araya G, Godoy I, Chiong M, Lavandero S, Jalil JE, Michea L (2014) Angiotensin-(1–9) reverses experimental hypertension and cardiovascular damage by inhibition of the angiotensin converting enzyme/Ang II axis. įlores-Munoz M, Work LM, Douglas K, Denby L, Dominiczak AF, Graham D, Nicklin SA (2012) Angiotensin-(1–9) attenuates cardiac fibrosis in the stroke-prone spontaneously hypertensive rat via the angiotensin type 2 receptor. ĭonoghue M, Hsieh F, Baronas E, Godbout K, Gosselin M, Stagliano N, Donovan M, Woolf B, Robison K, Jeyaseelan R, Breitbart RE, Acton S (2000) A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1–9. įorrester SJ, Booz GW, Sigmund CD, Coffman TM, Kawai T, Rizzo V, Scalia R, Eguchi S (2018) Angiotensin II signal transduction: an update on mechanisms of physiology and pathophysiology. Li XC, Zhang J, Zhuo JL (2017) The vasoprotective axes of the renin-angiotensin system: physiological relevance and therapeutic implications in cardiovascular, hypertensive and kidney diseases. Rajendran P, Rengarajan T, Thangavel J, Nishigaki Y, Sakthisekaran D, Sethi G, Nishigaki I (2013) The vascular endothelium and human diseases. Schwalm JD, McCready T, Lopez-Jaramillo P, Yusoff K, Attaran A, Lamelas P, Camacho PA, Majid F, Bangdiwala SI, Thabane L, Islam S, McKee M, Yusuf S (2019) A community-based comprehensive intervention to reduce cardiovascular risk in hypertension (HOPE 4): a cluster-randomised controlled trial. These findings may provide new insights for prevention and treatment of hypertension in future. Our study indicated Ang-(1–9) inhibited Ang II-induced hypertension through CNPY2/PERK pathway. Consistent with above effects in HUVECs, in Ang II-induced hypertensive mice, we found administration of exogenous Ang-(1–9) attenuated endothelial apoptosis and arterial blood pressure, which were mediated by CNPY2/PERK signaling pathway. ![]() Mechanically, Ang-(1–9) inhibited endothelial apoptosis by blocking CNPY2/PERK mediated CaMKII/Drp1-dependent mitochondrial fission and eIF2α/CHOP signal. In human umbilical vascular endothelial cells (HUVECs), we observed Ang-(1–9) inhibited Ang II-induced ERS associated endothelial apoptosis. Herein, we aimed to elucidate the effects of Ang-(1–9) on endothelial apoptosis and the underlying molecular mechanism in angiotensin II (Ang II) induced hypertension. Considering that the endothelial apoptosis was closely related to endoplasmic reticulum stress (ERS) and mitochondrial function. However, the mechanism of action remains unclear. Angiotensin-(1–9) (Ang-(1–9)) is a peptide of the counter-regulatory non-classical RAS with anti-hypertensive effects in vascular endothelial cells (ECs). Endothelial apoptosis caused by activation of renin-angiotensin system (RAS) plays a vital part in the occurrence and progress of hypertension.
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