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Evaluating sex-specific responses to western diet across the lifespan: impact on cardiac function and transcriptomic signatures in C57BL/6J mice at 530 and 640/750 days of age.
Cardiovasc Diabetol
December 2024
Cardiovascular Research Institute, Icahn School of Medicine at Mount Sinai, 1470 Madison Ave, s7-119, New York, NY, USA.
Background: Long-term consumption of Western Diet (WD) is a well-established risk factor for the development of cardiovascular disease (CVD); however, there is a paucity of studies on the long-term effects of WD on the pathophysiology of CVD and sex-specific responses.
Methods: Our study aimed to investigate the sex-specific pathophysiological changes in left ventricular (LV) function using transthoracic echocardiography (ECHO) and LV tissue transcriptomics in WD-fed C57BL/6 J mice for 125 days, starting at the age of 300 through 425 days.
Results: In female mice, consumption of the WD diet showed long-term effects on LV structure and possible development of HFpEF-like phenotype with compensatory cardiac structural changes later in life.
Cardio-metabolic and cytoskeletal proteomic signatures differentiate stress hypersensitivity in dystrophin-deficient mdx mice.
J Proteomics
December 2024
School of Biological Sciences, University of Canterbury, Christchurch 8041, New Zealand; Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Geelong, Australia; Department of Medicine, University of Otago, Christchurch 8014, New Zealand; Biomolecular Interaction Centre, School of Biological Sciences, University of Canterbury, Christchurch 8140, New Zealand; Maurice Wilkins Centre for Molecular Biodiscovery, Auckland 1010, New Zealand. Electronic address:
Extreme heterogeneity exists in the hypersensitive stress response exhibited by the dystrophin-deficient mdx mouse model of Duchenne muscular dystrophy. Because stress hypersensitivity can impact dystrophic phenotypes, this research aimed to understand the peripheral pathways driving this inter-individual variability. Male and female mdx mice were phenotypically stratified into "stress-resistant" or "stress-sensitive" groups based on their response to two laboratory stressors.
View Article and Find Full Text PDFJoint proteomic and metabolomic analysis reveals renal metabolic remodeling of chronic heart failure mice.
J Pharm Biomed Anal
December 2024
Institute of Traditional Chinese Medicine, Shaanxi Academy of Traditional Chinese Medicine, Xi'an, Shaanxi, China; Key Laboratory of TCM Drug Delivery, Shaanxi Academy of Traditional Chinese Medicine, Xi'an, Shaanxi, China. Electronic address:
Pharmacologic intervention in chronic heart failure (HF) with renal insufficiency is one of the clinical challenges due to the fact that the mechanisms of cardio-renal interactions in chronic heart failure (CHF) progressing have not been fully revealed. In this paper, C57BL/6 mice were applied thoracic aortic narrowing surgery to establish pressure overload CHF model. Cardiac function, serum markers, renal pathologic changes and kidney metabolism were analyzed at 4th, 8th, 12th, and 16th week after surgery respectively to evaluate the heart-Kidney pathologic overlap.
View Article and Find Full Text PDFApelin deficiency exacerbates cardiac injury following infarction by accelerating cardiomyocyte ferroptosis.
Free Radic Res
December 2024
Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Apelin is an endogenous ligand for the Apelin receptor and is a critical protective effector in myocardial infarction (MI). Nevertheless, these protective mechanisms are not fully understood. Ferroptosis is the major driving factor of MI.
View Article and Find Full Text PDFAneurysm Is Restricted by CD34 Cell-Formed Fibrous Collars Through the PDGFRb-PI3K Axis.
Adv Sci (Weinh)
December 2024
Department of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Aortic aneurysm is a life-threatening disease caused by progressive dilation of the aorta and weakened aortic walls. Its pathogenesis involves an imbalance between connective tissue repair and degradation. CD34 cells comprise a heterogeneous population that exhibits stem cell and progenitor cell properties.
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