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Intravenous injection of PCSK9 gain-of-function mutation in C57BL/6J background mice on Angiotensin II-induced AAA.
Biochim Biophys Acta Mol Basis Dis
January 2025
State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China. Electronic address:
Objective: This study was performed to compare the incidence of Angiotensin II (Ang II)-induced abdominal aortic aneurysms (AAA) between intravenous and intraperitoneal injection of AAV8.mPCSK9 in wild-type (WT) mice with C57BL/6J background and the pathological differences of above model in WT and ApoE mice.
Design: Male WT mice were injected intraperitoneally or intravenously with either a AAV8.
VSMC-specific TRPC1 deletion attenuates angiotensin II-induced hypertension and cardiovascular remodeling.
J Mol Med (Berl)
January 2025
Wuxi School of Medicine, Jiangnan University, Jiangsu Province, 1800 Lihu Rd, Wuxi, 214122, China.
Article Synopsis
- TRPC1 is a ion channel linked to cardiovascular issues, with increased expression observed in both treated vascular smooth muscle cells (VSMCs) and aortas of hypertensive mice.
- Lack of TRPC1 in VSMCs significantly reduces AngII-induced effects like vasoconstriction, hypertension, and heart changes, indicating its crucial role in these processes.
- The study identifies the EZH2-TRPC1-MEK/ERK pathway as a significant contributor to hypertension, suggesting that targeting TRPC1 or EZH2 could be effective in treating high blood pressure and related cardiovascular problems.
ClC-5 knockout mitigates angiotensin II-induced hypertension and endothelial dysfunction.
Life Sci
December 2024
Department of Pharmacology, Cardiac & Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, China. Electronic address:
Aims: Impairment of nitric oxide (NO) production is a major cause of endothelial dysfunction and hypertension. ClC-5 Cl channel is abundantly expressed in the vascular endothelium. However, it remains unclear how it regulates endothelial function.
View Article and Find Full Text PDFSirtuin 1 mediates the pro-survival effects of vitamin D in angiotensin II-induced hypertrophy of H9c2 cardiomyoblasts.
Mol Biol Rep
December 2024
Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Background: The role of 1,25-dihydroxyvitamin-D3 (VitD) and sirtuin-1 (SIRT1) in mitigating pathological cardiac remodeling is well recognized. However, the potential for SIRT1 to mediate the inhibitory effects of VitD on angiotensin II (Ang II) -induced hypertrophy in H9c2 cardiomyoblasts remains unclear.
Methods: H9c2 cardiomyoblasts were exposed to Ang II or a combination of VitD and Ang II, both in the absence and presence of SIRT1-specific siRNA.
Combination decoction of Astragalus mongholicus and mitigates pressure-overload cardiac dysfunction by inhibiting multiple ferroptosis pathways.
Front Pharmacol
December 2024
Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.
Background: Astragalus mongholicus (AM) and Salvia miltiorrhiza (SM) are commonly used in traditional Chinese medicine to treat heart failure (HF). Ferroptosis has been studied as a key factor in the occurrence of HF. It remains unclear whether the combined use of AM and SM can effectively improve HF and the underlying mechanisms.
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