Literature DB >> 16697925

Changes in cardiovascular function on treatment of inhibitors of apoptotic signal transduction pathways in left ventricular remodeling after myocardial infarction.

Tadashi Saitoh1, Takayuki Nakajima, Tatsuhisa Takahashi, Koichi Kawahara.   

Abstract

INTRODUCTION: It has been suggested that apoptosis in cardiac remodeling after myocardial infarction (MI) occurs in cardiomyocytes and is critically involved in the process of postinfarct cardiac remodeling. We investigated the pathophysiological link between myocardial apoptosis and cardiovascular function by modulating apoptotic signal transduction pathways.
METHODS: Either a caspase-3 inhibitor (CasI) or a calpain inhibitor (CalI) was administered immediately after MI in a rat model of MI. Blood pressure (BP), heart rate (HR), and blood flow velocity (BFV) were measured, and pressure-rate product (PRP) was calculated to estimate the changes in cardiovascular function (n=6 for each group).
RESULTS: BFV showed no remarkable changes in any of the groups. Both systolic blood pressure (SBP) and HR changed significantly (P<.01) in the MI+CasI and MI+CalI groups at 1 day after MI and returned to control levels thereafter. In contrast, SBP and HR remained significantly (P<.01) altered in the MI group. PRP in the MI groups was significantly decreased (P<.05 in the MI and MI+CasI groups; P<.01 in the MI+CalI group) at 1 day after MI and returned to control levels at 4 days.
CONCLUSION: This study suggests that inhibition of apoptosis during left ventricular remodeling ameliorates cardiovascular function in remodeled hearts.

Entities:  

Mesh:

Substances:

Year:  2006        PMID: 16697925     DOI: 10.1016/j.carpath.2006.01.003

Source DB:  PubMed          Journal:  Cardiovasc Pathol        ISSN: 1054-8807            Impact factor:   2.185


  6 in total

Review 1.  Role of various proteases in cardiac remodeling and progression of heart failure.

Authors:  Alison L Müller; Naranjan S Dhalla
Journal:  Heart Fail Rev       Date:  2012-05       Impact factor: 4.214

2.  Lack of beta3 integrin signaling contributes to calpain-mediated myocardial cell loss in pressure-overloaded myocardium.

Authors:  Geetha Suryakumar; Harinath Kasiganesan; Sundaravadivel Balasubramanian; Dhandapani Kuppuswamy
Journal:  J Cardiovasc Pharmacol       Date:  2010-06       Impact factor: 3.105

3.  Calpain inhibition preserves myocardial structure and function following myocardial infarction.

Authors:  Santhosh K Mani; Sundaravadivel Balasubramanian; Juozas A Zavadzkas; Laura B Jeffords; William T Rivers; Michael R Zile; Rupak Mukherjee; Francis G Spinale; Dhandapani Kuppuswamy
Journal:  Am J Physiol Heart Circ Physiol       Date:  2009-09-04       Impact factor: 4.733

Review 4.  Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.

Authors:  David Aluja; Sara Delgado-Tomás; Marisol Ruiz-Meana; José A Barrabés; Javier Inserte
Journal:  Int J Mol Sci       Date:  2022-04-07       Impact factor: 6.208

5.  Calpain-dependent cleavage of N-cadherin is involved in the progression of post-myocardial infarction remodeling.

Authors:  Yoko Kudo-Sakamoto; Hiroshi Akazawa; Kaoru Ito; Jiro Takano; Masamichi Yano; Chizuru Yabumoto; Atsuhiko T Naito; Toru Oka; Jong-Kook Lee; Yasushi Sakata; Jun-ichi Suzuki; Takaomi C Saido; Issei Komuro
Journal:  J Biol Chem       Date:  2014-06-02       Impact factor: 5.157

6.  Traditional Chinese medicine Qili qiangxin inhibits cardiomyocyte apoptosis in rats following myocardial infarction.

Authors:  Jun Xiao; Song-Bai Deng; Qiang She; Jun Li; Guo-Ying Kao; Jun-Sheng Wang; Y U Ma
Journal:  Exp Ther Med       Date:  2015-09-22       Impact factor: 2.447

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.