Article
Peripheral Vascular Disease
Caie Li, Liping Ma, Qiongying Wang, Xuejiao Shao, Lu Guo, Jianshu Chen, Wenjuan Wang, Jing Yu
Summary: The study reveals that the activation of the RhoA/ROCK signaling pathway may be involved in the development of hypertension induced by apatinib. Furthermore, the use of a nonspecific ROCK inhibitor, Y27632, shows potential in alleviating apatinib-induced hypertension.
JOURNAL OF HYPERTENSION
(2022)
Article
Integrative & Complementary Medicine
Ling Chen, Liquan Ren, Hongping Song, Hui Ren, Rong Xu, Xuying Huang
Summary: The study investigated the protective effects of triflavones from Selaginella doederleini against pulmonary hypertension (PH) in a rat model. Triflavones effectively reduced mPAP and arterial thickness, reversed increased proliferation and inhibited apoptosis induced by chronic hypoxia, and exhibited inhibitory effects on vascular remodeling through the PI3K/Akt signaling pathway.
ALTERNATIVE THERAPIES IN HEALTH AND MEDICINE
(2021)
Editorial Material
Immunology
Pin Li, Napoleone Ferrara
Summary: This study reveals the crosstalk between VEGF receptors in different organs and emphasizes the importance of VEGF receptor expression and interplay in vascular heterogeneity.
JOURNAL OF EXPERIMENTAL MEDICINE
(2022)
Review
Cell Biology
Qiang Zhao, Ping Song, Ming-Hui Zou
Summary: Pulmonary hypertension is a debilitating disease characterized by increased blood pressure in the pulmonary arteries. The role of AMPK in PH is controversial as both inhibition and activation of AMPK can potentially prevent the development of PH. Clinical studies suggest that metformin, an AMPK activator, is effective in treating early-stage PH and particularly beneficial for patients with PH associated with heart failure.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Medicine, Research & Experimental
Liyan Bai, Hae Jin Kee, Sin Young Choi, Young Mi Seok, Gwi Ran Kim, Seung-Jung Kee, Hyun Kook, Myung Ho Jeong
Summary: The genetic deletion of HDAC5 and treatment with class IIa HDAC inhibitors can prevent increases in blood pressure and arterial wall thickness induced by Ang II. HDAC5 plays a role in vascular contraction and hypertrophy, and its inhibition may be a potential target for hypertension treatment.
BIOMEDICINE & PHARMACOTHERAPY
(2021)
Article
Pharmacology & Pharmacy
Alejandro Gutierrez, Alfonso Gomez del Val, Cristina Contreras, Lucia Olmos, Ana Sanchez, Dolores Prieto
Summary: Abnormal endothelin-1 (ET-1) activity is involved in the pathogenesis of various vascular diseases. The inhibition of ET receptors has shown efficacy in clinical and experimental models. Peripheral resistance arteries play a key role in blood pressure regulation, and the study aimed to determine the Ca2+ signaling mechanisms involved in ET receptor-mediated vasoconstriction. ET-1-induced contraction in resistance arteries is mediated by the ETA receptor and involves Ca2+ mobilization, extracellular Ca2+ influx, and Ca2+ sensitization.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2023)
Article
Pharmacology & Pharmacy
Marieke Van Daele, Laura E. Kilpatrick, Jeanette Woolard, Stephen J. Hill
Summary: Vascular endothelial growth factor (VEGF) is crucial for angiogenesis and vascular endothelial cell functions. The study developed a ligand-binding assay to monitor the binding affinity and kinetics of different tyrosine kinase inhibitors (TKIs) to VEGF receptor 2 (VEGFR2). The results showed that compounds inhibiting the binding of a fluorescent analogue of sunitinib (sunitinib-red) also attenuated VEGFR2-mediated signaling, suggesting potential cardiovascular liabilities.
BIOCHEMICAL PHARMACOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Daria Monogiou Belik, Riccardo Bernasconi, Lifen Xu, Giacomo Della Verde, Vera Lorenz, Vivienne Gruterich, Melania Balzarolo, Michika Mochizuki, Otmar Pfister, Gabriela M. Kuster
Summary: This study aimed to test whether Flt3-targeting TKI treatment aggravates cardiac injury after myocardial infarction (MI). The results showed that quizartinib did not alter cardiac dimensions or function in healthy mice, but significantly enhanced ventricular dilatation and apoptotic cell death in MI mice. In vitro studies further confirmed that quizartinib increased cell death and apoptosis, potentially through a p38-dependent mechanism.
Article
Pharmacology & Pharmacy
Jingsi Zhang, Yuanshu Hui, Fengyi Liu, Qian Yang, Yi Lu, Yeting Chang, Qinlong Liu, Yanchun Ding
Summary: This study found that neohesperidin, as an antioxidant, can effectively inhibit hypertension and vascular remodeling induced by angiotensin II. The results of this study are of great significance for addressing global health problems.
FRONTIERS IN PHARMACOLOGY
(2022)
Review
Health Care Sciences & Services
Zhuangzhuang Jia, Shuai Wang, Haifeng Yan, Yawen Cao, Xuan Zhang, Lin Wang, Zeyu Zhang, Shanshan Lin, Xianliang Wang, Jingyuan Mao
Summary: Pulmonary vascular remodeling, involving changes in the intima, media and adventitia, is a critical structural alteration and pathological feature in pulmonary hypertension. It includes the proliferation and phenotypic transformation of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs), as well as interactions with pulmonary artery fibroblasts (PAFs) and extracellular matrix (ECM). Inflammatory mechanisms, apoptosis, and other factors are influenced by different mechanisms that contribute to disease progression. This article reviews these pathological changes and discusses the underlying mechanisms in the remodeling process.
JOURNAL OF PERSONALIZED MEDICINE
(2023)
Article
Oncology
Wenfeng Li, Wenjuan Chen, Hongyan Peng, Zhenghui Xiao, Jinqiao Liu, Yunhong Zeng, Ting Huang, Qingqing Song, Xun Wang, Yunbin Xiao
Summary: This study evaluated whether inhibiting the expression of pyruvate kinase M2 (PKM2) contributed to the improvement of pulmonary vascular remodeling in monocrotaline-induced pulmonary arterial hypertension (PAH) rats. Shikonin improved hemodynamics and pulmonary vascular remodeling in PAH rats, at least partly through the inhibition of PKM2 and the resultant suppression of aerobic glycolysis.
MOLECULAR MEDICINE REPORTS
(2023)
Article
Biochemistry & Molecular Biology
Luckika Panthiya, Jiraporn Tocharus, Amnart Onsa-ard, Waraluck Chaichompoo, Apichart Suksamrarn, Chainarong Tocharus
Summary: The study found that HHC can improve vascular function and attenuate vascular remodeling in hypertensive rats. Its potential mechanisms of action may involve antioxidant and anti-inflammatory effects.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2022)
Article
Biochemistry & Molecular Biology
Mariam Anis, Janae Gonzales, Rachel Halstrom, Noman Baig, Cat Humpal, Regaina Demeritte, Yulia Epshtein, Jeffrey R. Jacobson, Dustin R. Fraidenburg
Summary: In this study, we investigated the role of nmMLCK in the proliferation and migration of pulmonary arterial endothelial cells in the pathogenesis of PAH. We found that increased nmMLCK activity, along with increased ERK expression, may contribute to the development of PAH by stimulating cellular proliferation and migration.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Obstetrics & Gynecology
Jessica R. Zolton, Lindsey A. Sjaarda, Sunni L. Mumford, Elizabeth A. DeVilbiss, Keewan Kim, Kerry S. Flannagan, Jeannie G. Radoc, Neil J. Perkins, Robert M. Silver, Jean Wactawski-Wende, Micah J. Hill, Alan H. DeCherney, Enrique F. Schisterman
Summary: Circulating VEGF and sFLT-1 did not vary significantly across the menstrual cycle in normal ovulating women, and may not be useful as peripheral biomarkers of endometrial changes during the menstrual cycle. Plasma may be the preferred medium for measuring circulating VEGF in reproductive-age women, regardless of menstrual cycle phase.
OBSTETRICS AND GYNECOLOGY
(2021)
Article
Cardiac & Cardiovascular Systems
Congxia Bai, Ming Su, Yaohua Zhang, Yahui Lin, Yingying Sun, Li Song, Ning Xiao, Haochen Xu, Hongyan Wen, Meng Zhang, Jiedan Ping, Jing Liu, Rutai Hui, Hao Li, Jingzhou Chen
Summary: DNA methylation plays a crucial role in hypertension, with OVGP1 identified as a protein associated with hypertension that interacts with MYH9 to promote vascular remodeling and dysfunction.