Diazoxide postconditioning induces mitochondrial protein S-Nitrosylation and a redox-sensitive mitochondrial phosphorylation/translocation of RISK elements: no role for SAFE

Penna, Cláudia; Perrelli, Maria-Giulia; Tullio, Francesca; Angotti, Carmelina; Camporeale, Annalisa; Poli, Valeria; Pagliaro, Pasquale

doi:10.1007/s00395-013-0371-z

Cited by 46 publications

(55 citation statements)

References 88 publications

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“…Our recent finding that PostC with Diazoxide enhances S-nitrosylation, supports the idea that an appropriate redox environment is necessary for SNO-mediated cardioprotection 25,149,[203][204][205] .…”

Section: Is S-nitrosylation Important For Postconditioning's Protection?supporting

confidence: 75%

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Protein S-nitrosylation in preconditioning and postconditioning

Penna

Angotti

Pagliaro

2014

Exp Biol Med (Maywood)

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The coronary artery disease is a leading cause of death and morbidity worldwide. This disease has a complex pathophysiology that includes multiple mechanisms. Among these is the oxidative/nitrosative stress. Paradoxically, oxidative/nitrosative signaling plays a major role in cardioprotection against ischemia/reperfusion injury. In this context, the gas transmitter nitric oxide (NOֹ) may act through several mechanisms, such as guanylil cyclase activation and via Snitrosylation (SNO) of proteins. The latter is a covalent modification of a protein cysteine thiol by an NO-group that generates an S-nitrosothiol. Here we report data showing that NOֹ and SNO of proteins play a pivotal role not only in preconditioning, but also in postconditioning cardioprotection.

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Section: Is S-nitrosylation Important For Postconditioning's Protection?supporting

confidence: 75%

“…We should recall that PKC is also a target of PKG, thus further supporting a protective role of sGC/cGMP/PKG signaling. Whether PKG may target directly or indirectly PKC is a matter of debate 13,149,200,201 .…”

Section: Is S-nitrosylation Important For Postconditioning's Protection?mentioning

confidence: 99%

Protein S-nitrosylation in preconditioning and postconditioning

Penna

Angotti

Pagliaro

2014

Exp Biol Med (Maywood)

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“…There was however a statistically significant difference in infarct size following ischemic postconditioning, in which STAT3 knockout hearts had larger infarcts than their wild-type counterparts [49]. In fact, in a rat model, mitochondrial STAT3 activation was not observed with ischemia/reperfusion, but only with ischemic postconditioning [50]. While not studied in the context of ischemia, other studies have demonstrated that cardiac disease and injury is modulated by mitochondrial STAT3.…”

Section: Signal Transducer and Activator Of Transcription 3 (Stat3)mentioning

confidence: 99%

“…Whether similar events are modifying STAT3 in the mitochondria and if this has a functional significance remains to be determined [61]. Under these circumstances, recruitment of STAT3 to the mitochondria may involve both redox-dependent and redox-independent mechanisms [50], and thus, the mechanism by which STAT3 translocates to the mitochondria is likely stimulus dependent. More classical signaling cascades have also been linked to mitochondrial STAT3’s activation and protective effects in the heart.…”

Section: Signal Transducer and Activator Of Transcription 3 (Stat3)mentioning

confidence: 99%

Toward a new STATe: The role of STATs in mitochondrial function

Meier¹,

Larner²

2014

Seminars in Immunology

146

139

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Signal Transducers and Activators of Transcription (STATs) have been studied extensively and have been associated with virtually every biochemical pathway. Until recently, however, they were thought to exert these effects solely as a nuclear transcription factor. The finding that STAT3 localizes to the mitochondria and modulates respiration has opened up a new avenue through which STATs may regulate the cell. Recently, other members of the STAT family (STAT1, STAT2, STAT5, and STAT6) have also been shown to be present in the mitochondria. Coordinate regulation at the nucleus and mitochondria by these proteins places them in a unique position to drive cellular processes to achieve a specific response. This review summarizes recent findings that have led to our current understanding of how STATs influence mitochondrial function in health and disease.

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“…Myocardial ischemia is one of the main consequences of cardiovascular diseases [1] . Because of the lack of effective therapies, MI/R injury remains a major medical problem today [2] . Timely reperfusion is essential for recovery of the ischemic myocardium; however, reperfusion itself results in major cardiac damage [3,4] .…”

Section: Introductionmentioning

confidence: 99%