Hsp60 and heme oxygenase-1 (Hsp32) in acute myocardial infarction

Novo, Giuseppina; Cappello, Francesco; Rizzo, Manfredi; Fazio, Giovanni; Zambuto, Sabrina; Tortorici, Enza; Gammazza, Antonella Marino; Corrao, Simona; Zummo, Giovanni; Macario, Everly Conway de; Macario, Alberto J. L.; Assennato, Pasquale; Novo, Salvatore; Volti, Giovanni Li

doi:10.1016/j.trsl.2011.01.003

Cited by 64 publications

(61 citation statements)

References 51 publications

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“…Although this HSP60 reduction has yet to be explained, one can speculate that myolysis is accompanied by leakage of HSP60 and other proteins from damaged cells which then enter the circulation. This is in agreement with recent observations by our group in blood samples of patients with acute myocardial infarction, in which we found an increase of HSP60 levels that correlated positively with both troponin and creatine kinase activity [21]. However, the pathophysiological significance of HSP60 release from CMC after AF-induced myolysis has not yet been investigated.…”

Section: Hsp60 Increase In Atrial Fibrillation: Cause or Consequence?supporting

confidence: 93%

“…Coronary artery ligation induced an increase of HSP60 levels and this was related to a decrease of mitochondrial oxygen consumption rate in rats [19]. Myocardial infarction induced early release of HSP60 into the circulation, both in rats [20] and humans [21]. Elevated levels of circulating HSP60 were predictive of post-infarct adverse events [21], and thus this protein was proposed as a prognostic tool in postinfarct follow-up.…”

Section: Hsp60 Can Protect Cardiomyocytes From Ischaemia/reperfusion mentioning

confidence: 99%

“…Myocardial infarction induced early release of HSP60 into the circulation, both in rats [20] and humans [21]. Elevated levels of circulating HSP60 were predictive of post-infarct adverse events [21], and thus this protein was proposed as a prognostic tool in postinfarct follow-up. HSP60 levels did not change after a single episode of hypothermic ischaemia, cardioplegic arrest, and reperfusion in subjects undergoing cardiac surgery, and this may reflect the effective cardioprotection of extracorporeal circulation [22].…”

Section: Hsp60 Can Protect Cardiomyocytes From Ischaemia/reperfusion mentioning

confidence: 99%

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Heat Shock Protein-60 and Risk for Cardiovascular Disease

Rizzo¹,

Macario²,

Macario³

et al. 2011

CPD

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Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecular chaperones, 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 cytoprotective but a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examples of specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicate a pathogenic role for HSP60 but also its potential as a biomarker with applications for diagnosis, assessing prognosis and response to treatment, as well as for preventing and treating CVD.

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Section: Hsp60 Increase In Atrial Fibrillation: Cause or Consequence?supporting

confidence: 93%

Section: Hsp60 Can Protect Cardiomyocytes From Ischaemia/reperfusion mentioning

confidence: 99%

Section: Hsp60 Can Protect Cardiomyocytes From Ischaemia/reperfusion mentioning

confidence: 99%

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Heat Shock Protein-60 and Risk for Cardiovascular Disease

Rizzo¹,

Macario²,

Macario³

et al. 2011

CPD

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“…The actions of Hsp60 could lead to the modification of those proteins, and in this manner it could have a role in many diseases, including carcinogenesis. Heart Heart failure; Coronary vascular disease [137][138][139][140] Kidney Glomerulonephritis [141] Large bowel Inflammatory bowel diseases [19,142,143] Lung Chonic obstructive pulmonary disease [20] Oral cavity Periodontitis [144,145] Pancreas Type 1 diabetes [146][147][148][149][150][151] Skin Scleroderma, pemphigoid; Psoriasis; Dermatomyositis [152,153] Synovial joints Rheumatoid arthritis; Juvenile idiopathic arthritis [154][155][156][157] Vessels Vasculitis; Atherosclerosis [158][159][160][161][162][163][164][165][166][167] Adapted from [2]. Hsp60 seems to contribute to tumor cell survival, but this is controversial.…”

Section: Hsp60 Chaperonopathies and Chaperonotherapy: Targets And Agentsmentioning

confidence: 99%

Hsp60 chaperonopathies and chaperonotherapy: targets and agents

Cappello

Gammazza

Piccionello

et al. 2013

Expert Opinion on Therapeutic Targets

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133

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“…The increased Hsp32 expression in the present study was directly associated with decreased glutathione content in diethyl maleate-treated brain (Ewing and Maines 1993) and F − -exposed heart in rats. Increased levels of circulating Hsp60 were found in patients with acute myocardial infarction (AMI) suggesting a predictive marker for post-AMI adverse events (Novo et al 2011). In our study, the increased levels of Hsp60 expression in acute F − intoxication could be correlated with increased oxidative stress-mediated apoptosis in the myocardium .…”

Section: Resultsmentioning

confidence: 99%

Differential expression of myocardial heat shock proteins in rats acutely exposed to fluoride

Panneerselvam

Raghunath

2017

Cell Stress and Chaperones

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Acute fluoride (F − ) toxicity is known to cause severe cardiac complications and leads to sudden heart failure. Previously, we reported that increased myocardial oxidative damage, apoptosis, altered cytoskeleton and AMPK signaling proteins associated with energy deprivation in acute F − induced cardiac dysfunction. The present study was aimed to decipher the status of myocardial heat shock proteins (HspsHsp27, Hsp32, Hsp40, Hsp60, Hsp70, Hsp90) and heat shock transcription factor 1 (Hsf1) in acute F − -intoxicated rats. In order to study the expression of myocardial Hsps, male Wistar rats were treated with single oral doses of 45 and 90 mg/kg F − for 24 h. The expression levels of myocardial Hsps were determined using RT-PCR, western blotting, and immunohistochemical studies. Acute F − -intoxicated rats showed elevated levels of both the transcripts and protein expression of Hsf1, Hsp27, Hsp32, Hsp60, and Hsp70 when compared to control. In addition, the expression levels of Hsp40 and Hsp90 were significantly declined in a dosedependent fashion in F − -treated animals. Our result suggests that differential expression of Hsps in the rat myocardium could serve as a balance between pro-survival and death signal during acute F − -induced heart failure.

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Hsp60 and heme oxygenase-1 (Hsp32) in acute myocardial infarction

Cited by 64 publications

References 51 publications

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Hsp60 chaperonopathies and chaperonotherapy: targets and agents

Differential expression of myocardial heat shock proteins in rats acutely exposed to fluoride

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