Literature DB >> 12835952

Mitochondria and reperfusion injury. The role of permeability transition.

Fabio Di Lisa1, Marcella Canton, Roberta Menabò, Giuliano Dodoni, Paolo Bernardi.   

Abstract

The viability of the ischemic myocardium is jeopardized by alterations, such as ATP decrease and elevation in intracellular [Ca(2+)], that are related to derangements in mitochondrial function. Besides these established notions, the elucidation of the apoptotic cascade and the availability of novel methodologies for in situ studies prompted new interest in mitochondria. The characterization of mitochondrial channels provided a contribution that is particularly relevant to cardiovascular research. Here we focus on the role of the permeability transition pore by analyzing the methodological requirements for its characterization, the consequences of its opening and the possible relationships with other mitochondrial functions, especially with the K(ATP) channels.

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Year:  2003        PMID: 12835952     DOI: 10.1007/s00395-003-0415-x

Source DB:  PubMed          Journal:  Basic Res Cardiol        ISSN: 0300-8428            Impact factor:   17.165


  25 in total

Review 1.  Monoamine oxidases (MAO) in the pathogenesis of heart failure and ischemia/reperfusion injury.

Authors:  Nina Kaludercic; Andrea Carpi; Roberta Menabò; Fabio Di Lisa; Nazareno Paolocci
Journal:  Biochim Biophys Acta       Date:  2010-09-24

Review 2.  Cyclosporin variably and inconsistently reduces infarct size in experimental models of reperfused myocardial infarction: a systematic review and meta-analysis.

Authors:  W Y Lim; C M Messow; C Berry
Journal:  Br J Pharmacol       Date:  2012-04       Impact factor: 8.739

3.  Antidiabetic sulphonylureas activate mitochondrial permeability transition in rat skeletal muscle.

Authors:  Jolanta Skalska; Grazyna Debska; Wolfram S Kunz; Adam Szewczyk
Journal:  Br J Pharmacol       Date:  2005-07       Impact factor: 8.739

4.  Different mechanisms of mitochondrial proton leak in ischaemia/reperfusion injury and preconditioning: implications for pathology and cardioprotection.

Authors:  Sergiy M Nadtochiy; Andrew J Tompkins; Paul S Brookes
Journal:  Biochem J       Date:  2006-05-01       Impact factor: 3.857

5.  C-Jun N-terminal kinase 2 promotes graft injury via the mitochondrial permeability transition after mouse liver transplantation.

Authors:  T P Theruvath; C Czerny; V K Ramshesh; Z Zhong; K D Chavin; J J Lemasters
Journal:  Am J Transplant       Date:  2008-07-28       Impact factor: 8.086

6.  Minocycline and doxycycline, but not other tetracycline-derived compounds, protect liver cells from chemical hypoxia and ischemia/reperfusion injury by inhibition of the mitochondrial calcium uniporter.

Authors:  Justin Schwartz; Ekhson Holmuhamedov; Xun Zhang; Gregory L Lovelace; Charles D Smith; John J Lemasters
Journal:  Toxicol Appl Pharmacol       Date:  2013-09-05       Impact factor: 4.219

7.  Cyclosporin A in left ventricular remodeling after myocardial infarction.

Authors:  Andaleb Kholmukhamedov; Christina Logdon; Jiangting Hu; Richard A McKinney; Francis G Spinale; John J Lemasters; Rupak Mukherjee
Journal:  Am J Physiol Heart Circ Physiol       Date:  2013-10-25       Impact factor: 4.733

8.  Roles of endothelial nitric oxide synthase (eNOS) and mitochondrial permeability transition pore (MPTP) in epoxyeicosatrienoic acid (EET)-induced cardioprotection against infarction in intact rat hearts.

Authors:  Garrett J Gross; Anna Hsu; Adam W Pfeiffer; Kasem Nithipatikom
Journal:  J Mol Cell Cardiol       Date:  2013-02-16       Impact factor: 5.000

Review 9.  Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion.

Authors:  Giancarlo Solaini; David A Harris
Journal:  Biochem J       Date:  2005-09-01       Impact factor: 3.857

Review 10.  Mitochondrial reactive oxygen species production in excitable cells: modulators of mitochondrial and cell function.

Authors:  David F Stowe; Amadou K S Camara
Journal:  Antioxid Redox Signal       Date:  2009-06       Impact factor: 8.401

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