Results 1 to 10 of about 93,473 (332)

Lack of sexual dimorphism in a mouse model of isoproterenol-induced cardiac dysfunction.

open access: yesPLoS ONE, 2020
Sex-related differences in cardiovascular diseases are highly complex in humans and model-dependent in experimental laboratory animals. The objective of this work was to comprehensively investigate key sex differences in the response to acute and ...
Marianne K O Grant   +4 more
doaj   +2 more sources

Ginsenoside Re Improves Isoproterenol-Induced Myocardial Fibrosis and Heart Failure in Rats [PDF]

open access: hybridEvidence-Based Complementary and Alternative Medicine, 2019
Objective. Panax ginseng is used widely for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of P. ginseng.
Quanwei Wang   +4 more
semanticscholar   +2 more sources

Evaluation of Antioxidant and Immunity Activities of Quercetin in Isoproterenol-Treated Rats

open access: yesMolecules, 2012
The present study was designed to evaluate the effect of quercetin on myocardial oxidative stress and immunity function impairment induced by isoproterenol in rats.
Shaoping Lu, Lei Zhang, Hui Liu
doaj   +2 more sources

Low-dose l-isoproterenol versus salbutamol in hospitalized pediatric patients with severe acute exacerbation of asthma: A double-blind, randomized controlled trial

open access: goldAllergology International, 2019
Background: Although the guidelines in most countries do not recommend continuous inhalation of l-isoproterenol to treat pediatric patients with acute severe exacerbation of asthma, lower dose of l-isoproterenol has been widely used in Japan.
Toshio Katsunuma   +12 more
doaj   +2 more sources

Inhibition of Galectin-3 Pathway Prevents Isoproterenol-Induced Left Ventricular Dysfunction and Fibrosis in Mice [PDF]

open access: bronzeHYPERTENSION, 2016
G. Vergaro   +8 more
semanticscholar   +2 more sources

Selective HDAC8 Inhibition Attenuates Isoproterenol-Induced Cardiac Hypertrophy and Fibrosis via p38 MAPK Pathway

open access: yesFrontiers in Pharmacology, 2021
Histone deacetylase (HDAC) expression and enzymatic activity are dysregulated in cardiovascular diseases. Among Class I HDACs, HDAC2 has been reported to play a key role in cardiac hypertrophy; however, the exact function of HDAC8 remains unknown.
Tingwei Zhao   +5 more
semanticscholar   +1 more source

Exposure to Doxorubicin Modulates the Cardiac Response to Isoproterenol in Male and Female Mice

open access: yesPharmaceuticals, 2023
Sex is a salient risk factor in the development of doxorubicin-induced cardiotoxicity. Sex differences in the heart’s ability to respond to hypertrophic stimuli in doxorubicin-exposed animals have not been reported.
Kevin Agostinucci   +4 more
doaj   +1 more source

The β-blocker Nebivolol Is a GRK/β-arrestin Biased Agonist [PDF]

open access: yes, 2013
Nebivolol, a third generation β-adrenoceptor (β-AR) antagonist (β-blocker), causes vasodilation by inducing nitric oxide (NO) production. The mechanism via which nebivolol induces NO production remains unknown, resulting in the genesis of much of the ...
Andresen, Bradley T.   +9 more
core   +10 more sources

Klotho suppresses cardiomyocyte apoptosis in mice with stress-induced cardiac injury via downregulation of endoplasmic reticulum stress. [PDF]

open access: yesPLoS ONE, 2013
Cardiomyocyte apoptosis is a common pathological alteration in heart disease which results in systolic dysfunction or sudden death. Klotho is a novel anti-aging hormone.
Shuang Song   +4 more
doaj   +1 more source

Type 2 MI induced by a single high dose of isoproterenol in C57BL/6J mice triggers a persistent adaptive immune response against the heart

open access: yesJournal of Cellular and Molecular Medicine, 2020
Heart failure is the common final pathway of several cardiovascular conditions and a major cause of morbidity and mortality worldwide. Aberrant activation of the adaptive immune system in response to myocardial necrosis has recently been implicated in ...
E. Forte   +11 more
semanticscholar   +1 more source

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