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Endogenous hydrogen sulfide persulfidates endothelin type A receptor to inhibit pulmonary arterial smooth muscle cell proliferation.
Redox Biol
January 2025
Department of Pediatrics, Peking University First Hospital, Beijing, 100034, PR China. Electronic address:
Background: The binding of endothelin-1 (ET-1) to endothelin type A receptor (ETAR) performs a critical action in pulmonary arterial smooth muscle cell (PASMC) proliferation leading to pulmonary vascular structural remodeling. More evidence showed that cystathionine γ-lyase (CSE)-catalyzed endogenous hydrogen sulfide (HS) was involved in the pathogenesis of cardiovascular diseases. In this study, we aimed to explore the effect of endogenous HS/CSE pathway on the ET-1/ETAR binding and its underlying mechanisms in the cellular and animal models of PASMC proliferation.
View Article and Find Full Text PDFReviewing the path to balance: mechanisms and management of hypertension associated with targeting vascular endothelium in cancer therapy.
Hypertens Res
January 2025
The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China.
Contemporary anticancer drugs are often accompanied by varying degrees of cardiovascular toxicity, with hypertension emerging as one of the most prevalent side effects, particularly linked to inhibitors of vascular endothelial growth factor receptor (VEGFR) and tyrosine kinase inhibitors (TKIs). Hypertension induced by cancer therapies contributes to increased cardiovascular mortality in cancer patients and survivors. Given the shared common risk factors and overlapping pathophysiological mechanisms, hypertension is also a prevalent comorbidity in this patient population.
View Article and Find Full Text PDFSacubitril/valsartan reduces proteasome activation and cardiomyocyte area in an experimental mouse model of hypertrophy.
J Mol Cell Cardiol Plus
March 2024
Institute of Experimental Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany.
Sacubitril/valsartan (Sac/Val) belongs to the group of angiotensin receptor-neprilysin inhibitors and has been used for the treatment of heart failure (HF) for several years. The mechanisms that mediate the beneficial effects of Sac/Val are not yet fully understood. In this study we investigated whether Sac/Val influences the two proteolytic systems, the ubiquitin-proteasome system (UPS) and the autophagy-lysosomal pathway (ALP), in a mouse model of pressure overload induced by transverse aortic constriction (TAC) and in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) treated with endothelin-1 (ET1) serving as a human cellular model of hypertrophy.
View Article and Find Full Text PDFRepurposing bosentan as an anticancer agent: EGFR/ERK/c-Jun modulation inhibits NSCLC tumor growth.
Fundam Clin Pharmacol
February 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, 62514, Egypt.
Drug repurposing of well-established drugs to be targeted against lung cancer has been a promising strategy. Bosentan is an endothelin 1 (ET-1) blocker widely used in pulmonary hypertension. The current experiment intends to inspect the anticancer and antiangiogenic mechanism of bosentan targeting epidermal growth factor receptor (EGFR) /extra-cellular Signal Regulated Kinase (ERK) /c-Jun/vascular endothelial growth factor (VEGF) carcinogenic pathway.
View Article and Find Full Text PDFAbsence of Functional Autoantibodies Targeting Angiotensin II Type 1 Receptor (ATR) and Endothelin-1 Type A Receptor (ETR) in Circulation and Purified IgG from Patients with Systemic Sclerosis.
Arthritis Rheumatol
December 2024
Department of Rheumatology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands.
Objective: Systemic sclerosis (SSc) is a rare but severe autoimmune disease characterized by immune dysregulation, fibrosis, and vasculopathy. While previous studies have highlighted the presence of functional autoantibodies targeting the angiotensin II type 1 receptor (ATR) and endothelin-1 type A receptor (ETR), leading to autoantibody-mediated receptor stimulation and subsequent activation of endothelial cells (ECs), a comprehensive understanding of the direct interaction between these autoantibodies and their receptors is currently lacking. Moreover, existing data confirming the presence of these autoantibodies in SSc often rely on similar methodologies and assays.
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