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RESEARCH PRODUCT
Heat Shock Protein-60 and Risk for Cardiovascular Disease
Rizzo ManfrediGiovanni ZummoFrancesco CappelloGiovam Battista RiniEverly Conway De MacarioHeiner K. BertholdAlberto J.l. MacarioIoanna Gouni-bertholdsubject
Riskanimal structuresChaperonin Heat shock protein-60 cardiomyocytes heart failure cardiovascular diseases atherosclerosisChaperonin heat shock protein 60 cardiomyocytes heart failure cardiovascular disease atherosclerosis apoptosis microRNAs (miRs) diabetes Atrial fibrillationApoptosischemical and pharmacologic phenomenaDiseaseBioinformaticsAutoimmune DiseasesPathogenesisHeat shock proteinAtrial FibrillationDrug DiscoveryExtracellularAnimalsHumansMyocytes CardiacHeart FailurePharmacologybiologyfungiChaperonin 60AtherosclerosisResponse to treatmentCardiovascular DiseasesReperfusion InjuryChaperone (protein)HypertensionImmunologybiology.proteinHSP60Stress conditionsBiomarkersdescription
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecularchaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60,the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotectivebut a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examplesof specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicatea pathogenic role for HSP60 but also its potential as a biomarker with applications for diagnosis, assessing prognosis and response totreatment, as well as for preventing and treating CVD. © 2011 Bentham Science Publishers.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2011-01-01 | Current Pharmaceutical Design |