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Low-density lipoprotein receptor-related protein 6 ameliorates cardiac hypertrophy by regulating CTSD/HSP90α signaling during pressure overload.
Acta Pharmacol Sin
January 2025
Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, State Key Laboratory of Cardiovascular Diseases, NHC Key Laboratory of Ischemic Heart Diseases, and Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Pressure overload induces pathological cardiac remodeling, including cardiac hypertrophy and fibrosis, resulting in cardiac dysfunction or heart failure. Recently, we observed that the low-density lipoprotein receptor-related protein 6 (LRP6), has shown potential in enhancing cardiac function by mitigating cardiac fibrosis in a mouse model subjected to pressure overload. In this study, we investigated the role of LRP6 as a potential modulator of pressure overload-induced cardiac hypertrophy and elucidated the underlying molecular mechanisms.
View Article and Find Full Text PDFAnalysis of cardiac developmental toxicity induced by m-cresol in early life of zebrafish and its mechanism.
Comp Biochem Physiol C Toxicol Pharmacol
January 2025
Center for Clinical Medicine Research, First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, Jiangxi Province, China. Electronic address:
The compound m-Cresol, also referred to as 3-methylphenol,acts as a precursor in the creation of pesticides and plasticizers. This research has conducted a thorough evaluation of the toxic effects of m-cresol on the cardiac development of juvenile zebrafish, from 6 to 72 hpf. The study's results reveal that higher concentrations of m-Cresol, compared to lower ones, result in more severe heart abnormalities in zebrafish larvae.
View Article and Find Full Text PDFHypertrophic cardiomyopathy: insights into pathophysiology and novel therapeutic strategies from clinical studies.
Egypt Heart J
January 2025
Department of Physiology, Faculty of Basic Medical Sciences, Obafemi Awolowo College of Health Sciences, Olabisi Onabanjo University, Sagamu Campus, Sagamu, Ogun State, Nigeria.
Background: Hypertrophic cardiomyopathy (HCM) is a frequently encountered cardiac condition worldwide, often inherited, and characterized by intricate phenotypic and genetic manifestations. The natural progression of HCM is diverse, largely due to mutations in the contractile and relaxation proteins of the heart. These mutations disrupt the normal structure and functioning of the heart muscle, particularly affecting genes that encode proteins involved in the contraction and relaxation of cardiac muscle.
View Article and Find Full Text PDFThe N-Terminal Mutations of cMyBP-C Affect Calcium Regulation, Kinetics, and Force of Muscle Contraction.
Int J Mol Sci
December 2024
Institute of Immunology and Physiology, Russian Academy of Sciences, 620049 Yekaterinburg, Russia.
The cardiac myosin binding protein-C (cMyBP-C) regulates cross-bridge formation and controls the duration of systole and diastole at the whole heart level. As known, mutations in cMyBP-C increase the cross-bridge number and rate of their cycling, hypercontractility, and myocardial hypertrophy. We investigated the effects of the mutations D75N and P161S of cMyBP-C related to hypertrophic cardiomyopathy on the mechanism of force generation in isolated slow skeletal muscle fibers.
View Article and Find Full Text PDFHypertrophic Cardiomyopathy with Special Focus on Mavacamten and Its Future in Cardiology.
Biomedicines
November 2024
Department of Nephrocardiology, Medical University of Lodz, ul. Zeromskiego 113, 90-549 Lodz, Poland.
Hypertrophic cardiomyopathy (HCM) is a heterogeneous group of heart muscle disorders that affects millions, with an incidence from 1 in 500 to 1 in 200. Factors such as genetics, age, gender, comorbidities, and environmental factors may contribute to the course of this disease. Diagnosis of HCM has improved significantly in the past few decades from simple echocardiographic evaluations to a more complex, multimodal approach embracing advanced imaging, genetic, and biomarker studies.
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