2014
DOI: 10.1177/1753944714531638
|View full text |Cite
|
Sign up to set email alerts
|

Exploration of pharmacological interventions to prevent isoproterenol-induced myocardial infarction in experimental models

Abstract: High incidences of myocardial infarction associated with high morbidity and mortality, are a major concern and economic burden on industrialized nations. Persistent β-adrenergic receptor stimulation with isoproterenol leads to the development of oxidative stress, myocardial inflammation, thrombosis, platelet aggregation and calcium overload, which ultimately cause myocardial infarction. Therapeutic agents that are presently employed for the prevention and management of myocardial infarction are beta-blockers, … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
4
1

Citation Types

2
47
0

Year Published

2016
2016
2023
2023

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 50 publications
(49 citation statements)
references
References 111 publications
2
47
0
Order By: Relevance
“…Low Na + /K + -ATPase levels or activity promote Ca 2+ influx via NCX leading to Ca 2+ accumulation which can accelerate myocardial necrosis, contractile failure and also trigger arrhythmias. Calcium overload is one of the mechanisms of Iso-induced cardiac hypertrophy and heart failure ( Garg and Khanna, 2014 ) and also observed in our Iso treated H9C2 cells. Specifically, in cardiac hypertrophy, many studies have shown that Na + /K + pump function, and/or expression, is reduced.…”
Section: Discussionsupporting
confidence: 80%
“…Low Na + /K + -ATPase levels or activity promote Ca 2+ influx via NCX leading to Ca 2+ accumulation which can accelerate myocardial necrosis, contractile failure and also trigger arrhythmias. Calcium overload is one of the mechanisms of Iso-induced cardiac hypertrophy and heart failure ( Garg and Khanna, 2014 ) and also observed in our Iso treated H9C2 cells. Specifically, in cardiac hypertrophy, many studies have shown that Na + /K + pump function, and/or expression, is reduced.…”
Section: Discussionsupporting
confidence: 80%
“…Interestingly, GE treatment in this study restored Na + /K + -ATPase activity and Ca 2+ levels towards normal values possibly by protecting the membrane structures via its antioxidant activity and/or control of its gene activity. Ca 2+ accumulation was reported as one of the mechanisms inducing cardiac hypertrophy in a myocardial infarction model (Garg and Khanna 2014). Therefore, the present ability of GE to prevent Ca 2+ overload could be one of the causes of the lower HW/BW ratio observed in GE and GNT co-treated animals than that of the GNT-treated animals in this study.…”
Section: Discussionmentioning
confidence: 52%
“…This might be due to the activation of NF-kB by ISO. Activation of NF-kB occurs via β-Adrenergic receptor dependent pathway by ISO 38 . In inflammation and apoptosis, NF-kB acts as a key regulator.…”
Section: Discussionmentioning
confidence: 99%