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Cardiomyocyte and stromal cell cross-talk influences the pathogenesis of arrhythmogenic cardiomyopathy: a multi-level analysis uncovers DLK1-NOTCH pathway role in fibro-adipose remodelling.
Cell Death Discov
November 2024
Unit of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino IRCCS, 20138, Milan, Italy.
Arrhythmogenic Cardiomyopathy (ACM) is a life-threatening, genetically determined disease primarily caused by mutations in desmosomal genes, such as PKP2. Currently, there is no etiological therapy for ACM due to its complex and not fully elucidated pathogenesis. Various cardiac cell types affected by the genetic mutation, such as cardiomyocytes (CM) and cardiac mesenchymal stromal cells (cMSC), individually contribute to the ACM phenotype, driving functional abnormalities and fibro-fatty substitution, respectively.
View Article and Find Full Text PDFTranscriptome-wide N-methyladenosine methylation profile of atherosclerosis in mice.
BMC Genomics
December 2023
Department of Cardiology, Hainan Provincial Hospital of Traditional Chinese Medicine, 570203, Haikou, Hainan, P. R. China.
Background: Atherosclerosis (AS) is a critical pathological event during the progression of cardiovascular diseases. It exhibits fibrofatty lesions on the arterial wall and lacks effective treatment. N-methyladenosine (mA) is the most common modification of eukaryotic RNA and plays an important role in regulating the development and progression of cardiovascular diseases.
View Article and Find Full Text PDFAssociation of Tube Voltage With Plaque Composition on Coronary CT Angiography: Results From PARADIGM Registry.
JACC Cardiovasc Imaging
December 2021
Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, South Korea; Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea.
Objectives: This study sought to investigate the impact of low tube voltage scanning heterogeneity of coronary luminal attenuation on plaque quantification and characterization with coronary computed tomography angiography (CCTA).
Background: The impact of low tube voltage and coronary luminal attenuation on quantitative coronary plaque remains uncertain.
Methods: A total of 1,236 consecutive patients (age: 60 ± 9 years; 41% female) who underwent serial CCTA at an interval of ≥2 years were included from an international registry.
Using the Apolipoprotein E Knock-Out Mouse Model to Define Atherosclerotic Plaque Changes Induced by Low Dose Arsenic.
Toxicol Sci
November 2018
Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada.
Arsenic exposure increases the risk of atherosclerosis, the gradual occlusion of the large arteries with fibro-fatty plaque. While epidemiologic data provide convincing evidence this is true at higher exposures, it is unclear whether this may occur at low arsenic exposures, near the maximum contaminant level of 10 ppb. We have previously shown that 200 ppb arsenite in the drinking water increased the atherosclerosis in apolipoprotein E knock-out (apoE-/-) mice after 13 weeks, but the effects of lower concentrations were unknown.
View Article and Find Full Text PDFIncreased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophy.
Skelet Muscle
September 2017
Department of Anaesthesiology, Pharmacology & Therapeutics, University of British Columbia (UBC), 217-2176 Health Sciences Mall, Vancouver, British Columbia, V6T 1Z3, Canada.
Article Synopsis
- Duchenne muscular dystrophy (DMD) results from the loss of dystrophin and leads to severe mobility and heart issues, but the mdx mouse model only presents mild symptoms, prompting investigation into vascular factors.
- The study tested the effects of elevated lipid levels on muscle damage in mdx mice through dietary modifications, assessing heart and muscle function as well as blood lipid levels.
- Results indicated that mdx-ApoE mice, which had higher lipid levels, showed significant muscle pathology and ambulatory dysfunction reminiscent of human DMD, despite unchanged heart function and similar plaque deposition to ApoE mice.
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