The mitochondria as a target for cardioprotection in acute myocardial ischemia

Ertracht, Offir; Malka, Assaf; Atar, Shaul; Binah, Ofer

doi:10.1016/j.pharmthera.2013.11.003

Cited by 67 publications

(38 citation statements)

References 101 publications

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“…For example, NO-cGMPdependent sig nalling leads to opening of mitochondrial ATP sensitive potassium channels (K ATP channels) and reduced cal cium overload 82 . The protective effects of NO have also been attributed to their ability to inhibit the opening of mitochondrial permeability transition pores, which pre vents cytochrome c release and apoptosis 83 . In addition, NO inhibits complex I in the mitochondrial electron transport chain through secondary formation of nitrite and Snitrosothiols, thereby limiting mitochondrial ROS generation [84][85][86] .…”

Section: Mitochondrial Electron Transport Chainmentioning

confidence: 99%

Strategies to increase nitric oxide signalling in cardiovascular disease

Lundberg

Gladwin

Weitzberg

2015

Nat Rev Drug Discov

456

381

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Nitric oxide (NO) is a key signalling molecule in the cardiovascular, immune and central nervous systems, and crucial steps in the regulation of NO bioavailability in health and disease are well characterized. Although early approaches to therapeutically modulate NO bioavailability failed in clinical trials, an enhanced understanding of fundamental subcellular signalling has enabled a range of novel therapeutic approaches to be identified. These include the identification of: new pathways for enhancing NO synthase activity; ways to amplify the nitrate-nitrite-NO pathway; novel classes of NO-donating drugs; drugs that limit NO metabolism through effects on reactive oxygen species; and ways to modulate downstream phosphodiesterases and soluble guanylyl cyclases. In this Review, we discuss these latest developments, with a focus on cardiovascular disease.

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Section: Mitochondrial Electron Transport Chainmentioning

confidence: 99%

Strategies to increase nitric oxide signalling in cardiovascular disease

Lundberg

Gladwin

Weitzberg

2015

Nat Rev Drug Discov

456

381

View full text Add to dashboard Cite

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“…Mitochondria are the principal target of ischemic injury (15 The treatment of stroke is limited by a short therapeutic window and a lack of effective clinical drugs. Methylene blue (MB) has been used in laboratories and clinics since the 1890s.…”

Section: Introductionmentioning

confidence: 99%

Methylene Blue Reduces Acute Cerebral Ischemic Injury via the Induction of Mitophagy

Yao

Zhao

et al. 2015

Mol Med

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“…Mitochondrial dysfunction occurs early in the course of ischemia, leading to increased oxidative stress, cytochrome c release, and cardiomyocyte cell death. Mitochondria-targeting compounds have been actively pursued as potential drugs for cardioprotection in acute myocardial ischemia [8]. Resveratrol, an antioxidant and anti-inflammatory compound, protects brain tissues against I/R damage by inhibiting cardiomyocyte apoptosis [9].…”

Section: Introductionmentioning

confidence: 99%

TRAP1 Provides Protection Against Myocardial Ischemia-Reperfusion Injury by Ameliorating Mitochondrial Dysfunction

Peng

Dong

et al. 2015

Cell Physiol Biochem

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Background: Tumor necrosis factor receptor-associated protein 1 (TRAP1), an essential mitochondrial chaperone is induced in rat hearts following ischemia/reperfusion (I/R), but its role in myocardial I/R injury is unclear. The present study examined the function of TRAP1 in cardiomyocyte hypoxia/reoxygenation injury in vitro and myocardial I/R injury in vivo. Methods: HL-1 cardiomyocytes transfected with TRAP1 or vector were subjected to simulated I/R (SI/R) in vitro. Cell death and mitochondrial function were assessed. Wild type (WT) and TRAP1 knockout (TRAP1 KO) mice were subjected to cardiac I/R in vivo. The infarct size and myocardial apoptosis were determined. WT and TRAP1 KO cardiomyocytes were subjected to SI/R in vitro. Mitochondrial function was assessed. Results: TRAP1 overexpression protects HL-1 cardiomyocytes from SI/R-induced cell death in vitro. The reduced cell death was associated with decreased ROS generation, better-preserved mitochondrial ETC complex activity, membrane potential, and ATP production, as well as delayed mPTP opening. Loss of TRAP1 aggravates SI/R-induced mitochondrial damage in cardiomyocytes in vitro and myocardial I/R injury and apoptosis in vivo. Conclusion: The results of the present study show that TRAP1 provides cardioprotection against myocardial I/R by ameliorating mitochondrial dysfunction.

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The mitochondria as a target for cardioprotection in acute myocardial ischemia

Cited by 67 publications

References 101 publications

Strategies to increase nitric oxide signalling in cardiovascular disease

Strategies to increase nitric oxide signalling in cardiovascular disease

Methylene Blue Reduces Acute Cerebral Ischemic Injury via the Induction of Mitophagy

TRAP1 Provides Protection Against Myocardial Ischemia-Reperfusion Injury by Ameliorating Mitochondrial Dysfunction

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