Effects of angiotensin II blockade on cardiomyocyte regeneration after myocardial infarction in rats

Segersvärd, Heli; Lakkisto, Päivi; Forsten, Hanna; Immonen, Katariina; Kosonen, Riikka; Palojoki, Eeva; Kankuri, Esko; Harjula, Ari; Laine, Mika; Tikkanen, Ilkka

doi:10.1177/1470320313487567

Cited by 5 publications

(4 citation statements)

References 32 publications

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“…Although it is difficult to separate out the effect of Ang II on the satellite cell pool and its effect to reduce satellite cell proliferation and the relative contribution of each in vivo to the inhibition of regeneration, these data suggest that, in pathophysiological conditions of Ang II excess, normal muscle regenerative responses are blunted via an AT1R-mediated mechanism. It has been reported that AT1R blockers in LAD artery-ligated rodents have either no effect or modest effects on cardiac function (32)(33)(34)(35). Our data indicate that there was no significant improvement in cardiac function in response to candesartan in our experimental setting (Fig.…”

Section: Discussionmentioning

confidence: 46%

Angiotensin II Inhibits Satellite Cell Proliferation and Prevents Skeletal Muscle Regeneration

Yoshida

Galvez

Tiwari

et al. 2013

Journal of Biological Chemistry

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Background: Angiotensin II is elevated in cachexia and induces skeletal muscle atrophy. Results: Angiotensin inhibits muscle stem (satellite) cell proliferation via a Notch-dependent mechanism and depletes the satellite cell pool. Conclusion: Angiotensin prevents skeletal muscle regeneration by suppressing satellite cell function. Significance: This is the first report to show that satellite cells express angiotensin receptors and that angiotensin inhibits regeneration.

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Section: Discussionmentioning

confidence: 46%

Angiotensin II Inhibits Satellite Cell Proliferation and Prevents Skeletal Muscle Regeneration

Yoshida

Galvez

Tiwari

et al. 2013

Journal of Biological Chemistry

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“…Importantly, these metabolic changes were associated with cardiomyocyte hypertrophy, rather than hyperplasia. RAS playing a role in cardiomyocyte proliferation is unlikely given that its inhibition was not found to mediate cardiomyocyte proliferation post-MI, but did increase vascular densities in the border zone [ 193 ]. Consistently, upregulation of AT1 was found to decrease microvessel densities in the setting of MI, while its inhibition promoted angiogenesis [ 194 , 195 ].…”

Section: Discussionmentioning

confidence: 99%

Unravelling the Interplay between Cardiac Metabolism and Heart Regeneration

Fan

Cong

Yap

et al. 2023

IJMS

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Ischemic heart disease (IHD) is the leading cause of heart failure (HF) and is a significant cause of morbidity and mortality globally. An ischemic event induces cardiomyocyte death, and the ability for the adult heart to repair itself is challenged by the limited proliferative capacity of resident cardiomyocytes. Intriguingly, changes in metabolic substrate utilisation at birth coincide with the terminal differentiation and reduced proliferation of cardiomyocytes, which argues for a role of cardiac metabolism in heart regeneration. As such, strategies aimed at modulating this metabolism-proliferation axis could, in theory, promote heart regeneration in the setting of IHD. However, the lack of mechanistic understanding of these cellular processes has made it challenging to develop therapeutic modalities that can effectively promote regeneration. Here, we review the role of metabolic substrates and mitochondria in heart regeneration, and discuss potential targets aimed at promoting cardiomyocyte cell cycle re-entry. While advances in cardiovascular therapies have reduced IHD-related deaths, this has resulted in a substantial increase in HF cases. A comprehensive understanding of the interplay between cardiac metabolism and heart regeneration could facilitate the discovery of novel therapeutic targets to repair the damaged heart and reduce risk of HF in patients with IHD.

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“…There was a significant increase in group III when compared to I and IV group. This could be explained by the study of [28] that the ameliorating effect of SCs over that produced by LOS and also documented that LOS neither stimulated nor prevented cardiomyocyte regeneration.…”

Section: Discussionmentioning

confidence: 99%

Title: Comparative Histological Study on the Effect of Mesenchymal Stem Cell and Losartan on Cardiac Injury Induced by Doxorubicin in Male Albino rats.

Zaghloul

Elnour

Abdelfattah

et al. 2019

Egyptian Journal of Histology

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Introduction: Cardiovascular disease is the leading cause of death worldwide. Mesenchymal stem cells (MSCs) could be a promising therapy for treating cardiomyopathy. Aim of Work:To compare the therapeutic effects of MSCs and losartan (LOS) on doxorubicin (DOX) induced cardiomyopathy. Material and Methods: Thirty-nine male albino rats were divided into group I as a control group, group II received DOX 5 mg/kg ip once, group III received DOX as in group II `after 3 weeks LOS was given 30 mg/kg daily by gastric tube for 3 weeks and group IV received DOX as in group and after 3 weeks rats injected by 1ml of Paul Karl Haron (PKH)26 labeled MSCs iv. Blood samples were collected for estimating the creatine kinase-myocardial band (CK-MB) value. Cardiac muscle sections from all groups were examined by fluorescence microscope. All sections were processed for histological study using Hx&E and Masson's trichrome stains in addition to immunohistochemical staining for Cx43 and CD44.Morphometric and statistical studies were done. Results: Group II revealed fragmented muscle fibers and cytoplasmic vacuolation in addition to loss of transverse striation. These changes were confirmed by significant increase in the mean value of CK-MB and the mean area % of collagen fibers when compared to all other groups. In group III, regression of the previous changes was noticed and there was a significant decrease in the mean area % of collagen fibers when compared to group II. Group IV cardiomyocytes appeared healthy with normal arrangement and non-significant difference in mean area % of collagen fibers versus the control. Studying all groups immunohistochemically, revealed increase in positive reactions in LOS and SC groups when compared to DOX group with more increase in SC group than LOS group. Conclusion: Losartan improves cardiac injury with little effect on cardiac regeneration. MSCs have promising potential in cardiac regeneration.

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Effects of angiotensin II blockade on cardiomyocyte regeneration after myocardial infarction in rats

Cited by 5 publications

References 32 publications

Angiotensin II Inhibits Satellite Cell Proliferation and Prevents Skeletal Muscle Regeneration

Angiotensin II Inhibits Satellite Cell Proliferation and Prevents Skeletal Muscle Regeneration

Unravelling the Interplay between Cardiac Metabolism and Heart Regeneration

Title: Comparative Histological Study on the Effect of Mesenchymal Stem Cell and Losartan on Cardiac Injury Induced by Doxorubicin in Male Albino rats.

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