SIRT5 and post-translational protein modifications: A potential therapeutic target for myocardial ischemia-reperfusion injury with regard to mitochondrial dynamics and oxidative metabolism

Zou, Rongjun; Shi, Wu; Tao, Jun; Li, Hongmu; Lin, Xuemei; Yang, Songran; Hua, Peng

doi:10.1016/j.ejphar.2017.11.005

Cited by 32 publications

(28 citation statements)

References 124 publications

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“…The role for SIRT5 as a metabolic and inflammatory regulator is still emerging. The literature indicates that SIRT5 regulates ischemia reperfusion injury in heart and brain and has a role in cancer [ 141 , 146 , 147 ].…”

Section: Sirtuins and Sepsis Immuno-metabolismmentioning

confidence: 99%

Sirtuins and Immuno-Metabolism of Sepsis

Wang

Buechler

Woodruff

et al. 2018

IJMS

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Sepsis and septic shock are the leading causes of death in non-coronary intensive care units worldwide. During sepsis-associated immune dysfunction, the early/hyper-inflammatory phase transitions to a late/hypo-inflammatory phase as sepsis progresses. The majority of sepsis-related deaths occur during the hypo-inflammatory phase. There are no phase-specific therapies currently available for clinical use in sepsis. Metabolic rewiring directs the transition from hyper-inflammatory to hypo-inflammatory immune responses to protect homeostasis during sepsis inflammation, but the mechanisms underlying this immuno-metabolic network are unclear. Here, we review the roles of NAD+ sensing Sirtuin (SIRT) family members in controlling immunometabolic rewiring during the acute systemic inflammatory response associated with sepsis. We discuss individual contributions among family members SIRT 1, 2, 3, 4 and 6 in regulating the metabolic switch between carbohydrate-fueled hyper-inflammation to lipid-fueled hypo-inflammation. We further highlight the role of SIRT1 and SIRT2 as potential “druggable” targets for promoting immunometabolic homeostasis and increasing sepsis survival.

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Section: Sirtuins and Sepsis Immuno-metabolismmentioning

confidence: 99%

Sirtuins and Immuno-Metabolism of Sepsis

Wang

Buechler

Woodruff

et al. 2018

IJMS

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“…In the heart, SIRT5 functions as a regulator of fatty acid metabolism, oxidative phosphorylation, and other metabolic pathways. [ 54 55 56 ] SIRT5 knockout (SIRT5 KO) mice were shown to be more susceptible to ischemia/reperfusion (I/R) injury, mainly due to a heightened rate of succinate oxidation catalyzed by succinate dehydrogenase (SDH) during reperfusion. [ 54 ] Succinate has been found to increase substantially in the heart, brain, and other tissues following ischemia.…”

Section: Sirt5 Regulates Several Metabolic Processes During Ischemiamentioning

confidence: 99%

“…Sirt5 deficient MEFs showed higher ROS levels, suggesting a protective role in oxidative stress for SIRT5. [ 56 ] This was due to a decrease in the production of NADPH, an essential cofactor involved in maintaining glutathione in its reduced form (GSH). GSH acts as an antioxidant, ROS scavenger, and when reduced results in ROS accumulation.…”

Section: Sirt5 Regulates Several Metabolic Processes During Ischemiamentioning

confidence: 99%

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Effects of ischemic preconditioning on mitochondrial and metabolic neruoprotection: 5' adenosine monophosphate-activated protein kinase and sirtuins

Jackson

Escobar

et al. 2018

Brain Circ

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Stroke and cardiac arrest result in cerebral ischemia, a highly prevalent medical issue around the world, which is characterized by a reduction or loss of blood flow to the brain. The loss of adequate nutrient supply in the brain during ischemia results in neuronal cell death contributing to cognitive and motor deficits that are usually permanent. Current effective therapies for cerebral ischemia are only applicable after the fact. Thus, the development of preventative therapies of ischemia is imperative. A field of research that continues to show promise in developing therapies for cerebral ischemia is ischemic preconditioning (IPC). IPC is described as exposure to sublethal ischemic events, which induce adaptive changes that provide tolerance to future ischemic events. Through either transient sub-lethal ischemic events, or the actions of a preconditioning molecular mimetic, IPC typically results in augmented gene expression and cellular metabolism. A pivotal target of such changes in gene expression and metabolism is the mitochondrion. Direct and indirect effects on mitochondria by IPC can result in the activation of 5’ adenosine monophosphate-activated protein kinase (AMPK), a master regulator of cellular metabolism. Changes in the activity of the posttranslational modifiers, SIRT1 and SIRT5, also contribute to the overall adaptive processes in cellular metabolism and mitochondrial functioning. In this review, we present recently collected evidence to highlight the neuroprotective interactions of mitochondria with AMPK, SIRT1, and SIRT5 in IPC. To produce this review, we utilized PubMed and previous reviews to target and to consolidate the relevant studies and lines of evidence.

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“…Cardiovascular dysfunction, including acute myocardial infarction and cardiac failure, is a leading cause of morbidity and mortality worldwide. Common treatment strategies for cardiovascular disease include pharmacological intervention, mechanical coronary reperfusion, and surgery [1]. Transient occlusion of a coronary artery damages myocardial cells because of ischemic insult and energy exhaustion; however, the reperfusion of blood to myocardium also causes severe tissue injury, called ischemia-reperfusion (I/R) injury [1][2][3].…”

Section: Introductionmentioning

confidence: 99%

Gypenosides protect against cardiac ischemia-reperfusion injury by inhibiting mitochondria-dependent apoptosis

Qiao¹,

Liu²,

Chen³

2018

Trop. J. Pharm Res

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Purpose:To investigate the effect of gypenoside (Gyp) on myocardial ischemia-reperfusion (I/R), focusing on mitochondrial function and oxidative stress. Methods: A 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide methylthiazolyldiphenyltetrazolium bromide (MTT) assay was employed to measure the protective effect of Gyp pre-treatment against I/R injury. Flow cytometry was used to detect cellular reactive oxygen species (ROS) content and mitochondrial membrane potential (MMP) levels. Additionally, cytochrome C release was observed by laser scanning confocal microscopy. Finally, Annexin V staining and western blot were applied to analyse cell apoptosis. Results: MTT assay results showed that Gyp pre-treatment protected H9C2 cells against I/R injury in a Gyp concentration-dependent manner. Moreover, Gyp treatment inhibited intracellular ROS production, repressed cytochrome C transposition induced by I/R treatment, and recovered MMP to almost normal levels. Furthermore, the expression of apoptosis-related proteins included cleaved caspase-3, -9 and Bax which were decreased by Gyp treatment after I/R injury. Conclusion: These results suggest that Gyp treatment prior to injury can help maintain normal mitochondrial function and inhibit ROS production during I/R injury, ultimately leading to the suppression of I/R-induced cell apoptosis. Thus, Gyp may be a promising drug for the treatment of myocardial I/R. This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest

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SIRT5 and post-translational protein modifications: A potential therapeutic target for myocardial ischemia-reperfusion injury with regard to mitochondrial dynamics and oxidative metabolism

Cited by 32 publications

References 124 publications

Sirtuins and Immuno-Metabolism of Sepsis

Sirtuins and Immuno-Metabolism of Sepsis

Effects of ischemic preconditioning on mitochondrial and metabolic neruoprotection: 5' adenosine monophosphate-activated protein kinase and sirtuins

Gypenosides protect against cardiac ischemia-reperfusion injury by inhibiting mitochondria-dependent apoptosis

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