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| http://dx.doi.org/10.5152/TJAR.2021.1002 | DOI Listing |
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Xinkeshu formula restrains pathological cardiac hypertrophy through metabolic remodeling via AMPK/mTOR pathway.
Phytomedicine
January 2025
Department of Cardiology, Pukou Hospital of Chinese Medicine affiliated to China Pharmaceutical University, Nanjing, PR China; Jiangsu Key Laboratory for Functional Substance of Chinese Medicine, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, PR China. Electronic address:
Background: Xinkeshu (XKS) formula is a patented traditional Chinese medicine used to treat cardiovascular diseases for decades. However, little is known about its potential influence on heart metabolism under pathological conditions.
Purpose: This study sought to explore the potential role of XKS in pathological cardiac hypertrophy, with a focus on metabolic remolding.
Atractylenolide-III restrains cardiac fibrosis after myocardial infarction via suppression of the RhoA/ROCK1 and ERK1/2 pathway.
Int Immunopharmacol
January 2025
Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Hubei Key Laboratory of Biological Targeted Therapy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, China; Hubei Engineering Research Center for Immunological Diagnosis and Therapy of Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, China. Electronic address:
Background: Cardiac fibrosis, a critical factor in myocardial remodeling post-myocardial infarction (MI), can advance heart failure progression. Atractylenolide III (ATL-III), derived from Atractylodes lancea, has recognized antioxidant and anti-inflammatory effects; however, its influence on cardiac fibrosis remains unclear.
Methods: MI was induced in mice by permanent ligation of the left anterior descending (LAD) coronary artery, followed by 2 weeks of ATL-III or dimethyl sulfoxide (DMSO) treatment.
Correlation of Pseudocholinesterase Level with Clinical, Biochemical Parameters Including Cardiac Profile and the Outcome in Organophosphorus Poisoning.
Ann Afr Med
October 2024
Department of Forensic Medicine, KGMU, Lucknow, Uttar Pradesh, India.
Background: Poisoning is a significant health hazard and a leading cause of morbidity and mortality worldwide. India, being a predominantly agrarian country, routinely employs organophosphate (OP) pesticides in farming, and they are readily available "over the counter." OPs exert their toxicity by interfering with the normal function of acetylcholine, an essential neurotransmitter throughout the autonomic and central nervous systems.
View Article and Find Full Text PDFEchocardiographic evaluation in koi carp (Cyprinus carpio) under manual restraint compared to anesthesia with isoeugenol.
Am J Vet Res
October 2024
Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA.
Objective: To establish an echocardiographic technique in koi carp (Cyprinus carpio), compare cardiopulmonary parameters under manual restraint versus anesthesia, and provide a gross anatomical and histologic cardiac description.
Methods: A randomized, crossover echocardiography study was performed in 40 clinically healthy adult, unknown sex, privately owned koi carp on May 10 and 11 through June 26 and 27, 2021. Echocardiography was examined for each koi under manual restraint and isoeugenol at 50 ppm, with 3 measurements per examination performed by a radiologist and cardiologist.
Fibroblast Smad7 Induction Protects the Remodeling Pressure-Overloaded Heart.
Circ Res
July 2024
Department of Medicine (Cardiology), Wilf Family Cardiovascular Research Institute (C.H., A.V.S., I.T., S.C.H., A.H., S.H., H.V., N.G.F.), Indiana University School of Medicine, Indianapolis.
Background: Cardiac fibroblast activation contributes to adverse remodeling, fibrosis, and dysfunction in the pressure-overloaded heart. Although early fibroblast TGF-β (transforming growth factor-β)/Smad (small mother against decapentaplegic)-3 activation protects the pressure-overloaded heart by preserving the matrix, sustained TGF-β activation is deleterious, accentuating fibrosis and dysfunction. Thus, endogenous mechanisms that negatively regulate the TGF-β response in fibroblasts may be required to protect from progressive fibrosis and adverse remodeling.
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