Results 171 to 180 of about 93,083 (312)

Prediabetic cardiomyopathy is attenuated by hypothalamic PVN oxytocin neuron activation

The Journal of Physiology, EarlyView.
Abstract figure legend A long‐term high‐fat, high‐fructose diet induces prediabetes with insulin resistance, hyperinsulinaemia, elevated triglycerides and metabolic‐associated steatotic liver disease (MASLD) in male rats. Animals developed prediabetic cardiomyopathy characterized by diastolic dysfunction, interstitial fibrosis and tachycardia ...
Anna Nilsson, Joan Escobar, Kira Kuraoka, Ian Venter, Cielo A. Carnate, Matthew W. Kay, David Mendelowitz, Kathryn J. Schunke   +7 more
wiley   +1 more source

Loss of DNA repair mechanisms in cardiac myocytes induce dilated cardiomyopathy. [PDF]

Aging Cell, 2023
Henpita C, Vyas R, Healy CL, Kieu TL, Gurkar AU, Yousefzadeh MJ, Cui Y, Lu A, Angelini LA, O'Kelly RD, McGowan SJ, Chandrasekhar S, Vanderpool RR, Hennessy-Wack D, Ross MA, Bachman TN, McTiernan C, Pillai SPS, Ladiges W, Lavasani M, Huard J, Beer-Stolz D, St Croix CM, Watkins SC, Robbins PD, Mora AL, Kelley EE, Wang Y, O'Connell TD, Niedernhofer LJ.   +29 more
europepmc   +1 more source

Angiotensin‐converting enzyme and exercise adaptations: Genetic variability, pharmacological modulation and future directions

The Journal of Physiology, EarlyView.
Abstract figure legend ACE I/D genotype, enzyme activity and integrated physiological adaptations. Upper panel: Conceptual framework linking the ACE I/D polymorphism (left) with circulating/tissue ACE activity (centre; violin plots based on hypothetical data for illustration) and strength/power versus endurance phenotypes (right).
Tórur Sjúrðarson, Nikolai B. Nordsborg   +1 more
wiley   +1 more source

Iron regulation in neonatal rat cardiac myocytes

, 1997
grantor: University of TorontoCardiac iron overload is the major cause of morbidity and mortality in iron-loading diseases. Iron-induced cardiac dysfunction can be mimicked in vitro using cultures of iron-loaded neonatal rat cardiac myocytes ...
Sirna, Josephine Barbara
core   +1 more source

Engineering Human Myocardium: Integrating the Maturation of hiPSC-Derived Cardiac Myocytes Across Genetic, Structural, Physiological and Multicellular Systems. [PDF]

Cells
Hosny N, Cohen H, Bauer J, Schreifels J, Lin R, Thompson BR, Metzger JM.   +6 more
europepmc   +1 more source

A-Kinase Anchoring Proteins in Cardiac Myocytes and Their Roles in Regulating Calcium Cycling. [PDF]

Cells, 2023
Subramanian H, Nikolaev VO.
europepmc   +1 more source

Ro5‐4864, a ligand of the mitochondrial translocator protein, protects against heart failure in mice via regulation of the p62‐Keap1‐Nrf2 axis

The Journal of Physiology, EarlyView.
Abstract figure legend Graphical abstract of the proposed Ro5‐4864 mechanism of action via p62‐Keap1‐Nrf2 axis in heart failure. TSPO, the 18‐kDa mitochondrial translocator protein of the outer mitochondrial membrane, can directly interact with p62 (also known as SQSTM1), which is crucial for the degradation of damaged mitochondria by autophagy ...
Daphne A. Diloretto, Phung N. Thai, Gabriela Grigorean, Veneese J. Brown, Tjien Dwyer, Nipavan Chiamvimonvat, Elena N. Dedkova, Saul Schaefer   +7 more
wiley   +1 more source

[Expression of Concern] Novel insights into the role of HSP90 in cytoprotection of H₂S against chemical hypoxia‑induced injury in H9c2  cardiac myocytes. [PDF]

Int J Mol Med
Yang Z, Yang C, Xiao L, Liao X, Lan A, Wang X, Guo R, Chen P, Hu C, Feng J.   +9 more
europepmc   +1 more source

Necrotic cardiac myocytes skew macrophage polarization towards a classically activated phenotype. [PDF]

PLoS One, 2023
Jiang W, Adamo L, Lim K, Matkovich SJ, Evans S, Rocha-Resende C, Mann DL.   +6 more
europepmc   +1 more source

The role of bone marrow derived cells in cardiac repair

, 2012
PhDCurrent pharmacological therapies fail to address the final end-point of cardiac ischaemia — the death and dysfunction of cardiomyocytes. Advances in stem cell biology have provided hope, for the first time, of addressing this underlying pathology.
Lovell, Matthew J, Lovell, Matthew J.
core