2009
DOI: 10.1111/j.1752-8062.2009.00163.x
|View full text |Cite
|
Sign up to set email alerts
|

Divergent Effects of Losartan and Metoprolol on Cardiac Remodeling, C‐kit+ Cells, Proliferation and Apoptosis in the Left Ventricle after Myocardial Infarction

Abstract: Introduction Th e activation of the renin-angiotensin-aldosterone system and sympathetic hyperactivation play central roles in pathogenesis of postinfarction left ventricular (LV) remodeling and heart failure. Th is understanding has provided strong therapeutic rationale for using angiotensin converting enzyme (ACE) inhibitors and beta-blockers in patients with myocardial infarction (MI). 1,2 However, data supporting the use of angiotensin receptor blockers (ARBs) for the primary prevention of myocardial infar… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
14
0

Year Published

2012
2012
2021
2021

Publication Types

Select...
8
1

Relationship

1
8

Authors

Journals

citations
Cited by 16 publications
(14 citation statements)
references
References 52 publications
0
14
0
Order By: Relevance
“…Metoprolol did not affect collagen deposition, matrix metalloproteinase 9, or tissue inhibitor of metalloproteinase 1 expression in the current study, but metoprolol has been shown to attenuate adverse remodeling postmyocardial infarction by increasing the number of c-kit + cells. 9 This indicates that ivabradine and metoprolol exert cardiac protective roles, through distinct mechanisms that may be modified under different conditions.…”
mentioning
confidence: 99%
“…Metoprolol did not affect collagen deposition, matrix metalloproteinase 9, or tissue inhibitor of metalloproteinase 1 expression in the current study, but metoprolol has been shown to attenuate adverse remodeling postmyocardial infarction by increasing the number of c-kit + cells. 9 This indicates that ivabradine and metoprolol exert cardiac protective roles, through distinct mechanisms that may be modified under different conditions.…”
mentioning
confidence: 99%
“…For example, metoprolol reduced myocyte hypertrophy and collagen deposition in a rat model of renovascular hypertension-induced cardiac hypertrophy [29]. Moreover, Serpi et al [30] suggested that metoprolol treatment attenuated adverse remodeling via decreased apoptosis and fibrosis in the peri-infarct region in a model of coronary ligation in rats. Thus, based on our study, it was worth noting that metoprolol could reverse chronic OSAinduced structural remodeling.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, it can be postulated that the utility of AT1R blockage and AT2R agonist may improve the impaired growth reserve and decrease susceptibility to apoptosis of CSCs. However, it is metoprolol rather than losartan that can increase the number of c-kit POS CSCs following MI treatment [24]. …”
Section: Strategies To Activate Cscs In Situmentioning
confidence: 99%
“…We have observed that the activation of an endogenous reserve of CSCs niches is one of the most important mechanisms of mesenchymal stem cell (MSC)-mediated cardiac repair after MI [1]. Accumulating evidence has also demonstrated that the resident CSC pool may be activated by adjacent cells via cell-to-cell interactions, local growth factor administration, microRNA (miRNA, miR) modulators and pharmaceutical preparations and others, to reconstitute dead myocardial tissue and recover cardiac function [1,18,20,[23][24][25][26].…”
Section: Introductionmentioning
confidence: 99%