Loss of PINK1 increases the heart's vulnerability to ischemia-reperfusion injury

Autor: Marthe H.R. Ludtmann, Plamena R. Angelova, Hilary K. Siddall, Sang Bing Ong, Sean M. Davidson, Andrew R. Hall, Niall Burke, Derek J. Hausenloy, Derek M. Yellon, Emma Deas, Mihaela M. Mocanu, Uma A. Mukherjee
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Pathology
Mouse
Myocardial Infarction
lcsh:Medicine
Coronary Artery Disease
Mitochondrion
medicine.disease_cause
Cardiovascular
Mitochondrial Membrane Transport Proteins
Gene Knockout Techniques
Mice
Molecular Cell Biology
Signaling in Cellular Processes
Myocytes
Cardiac
Inner mitochondrial membrane
lcsh:Science
Apoptotic Signaling Cascade
Apoptotic Signaling
Membrane Potential
Mitochondrial
Multidisciplinary
Cell Death
Dopaminergic
Antiapoptotic Signaling
Animal Models
Signaling Cascades
Mitochondria
Reperfusion Injury
Cardiology
Medicine
Disease Susceptibility
Research Article
Signal Transduction
medicine.medical_specialty
Ischemia
PINK1
Biology
Cell Line
Model Organisms
Internal medicine
medicine
Animals
Mitochondrial Permeability Transition Pore
Myocardium
lcsh:R
medicine.disease
Oxygen
Oxidative Stress
Mitochondrial permeability transition pore
lcsh:Q
Reperfusion injury
Protein Kinases
Oxidative stress
Zdroj: PLoS ONE, Vol 8, Iss 4, p e62400 (2013)
PLoS ONE
ISSN: 1932-6203
Popis: Objectives Mutations in PTEN inducible kinase-1 (PINK1) induce mitochondrial dysfunction in dopaminergic neurons resulting in an inherited form of Parkinson’s disease. Although PINK1 is present in the heart its exact role there is unclear. We hypothesized that PINK1 protects the heart against acute ischemia reperfusion injury (IRI) by preventing mitochondrial dysfunction. Methods and Results Over-expressing PINK1 in HL-1 cardiac cells reduced cell death following simulated IRI (29.2±5.2% PINK1 versus 49.0±2.4% control; N = 320 cells/group P5 animals/group; P
Databáze: OpenAIRE
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