SIRT3 protects cardiomyocytes from oxidative stress-mediated cell death by activating NF-κB

Chen, Chun-Juan; Fu, Yucai; Yu, Wei; Wang, Wei

doi:10.1016/j.bbrc.2012.11.066

Cited by 112 publications

(84 citation statements)

References 22 publications

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“…Expression of SIRT3 is upregulated in response to stress and its overexpression has a protective role for cardiomyocytes from stress-mediated cell death by deacetylating Ku70 and preventing translocation of BAX to mitochondria [91]. Additionally, SIRT3 overexpression protects cardiomyocytes from oxidative stress by downregulating apoptosis regulator BAX and BCL-2 by inducing NF-κB transcription factor [24].…”

Section: Changes In Sirtuin 3 Expression In Carcinogenesismentioning

confidence: 99%

“…Metformin, which is a drug used for the treatment of diabetes, upregulates the expression of SIRT3 in about 8 weeks old mice with heart failure after myocardial infarction [103]. It was suggested that metformin-mediated SIRT3 upregulation and deacetylation of PGC-1α increase mitochondrial ATP production and mitochondrial oxygen consumption rates in the [24,102] Metformin N/A PGC-1α Stimulates mitochondrial ATP production and oxygen consumption rates [103] Adjudin N/A IDH2 Scavenges mtROS [96,97] RIP140 (SIRT3 repressing TF) ERRα LCAD Increases mtROS and lipid accumulation [92,101] MnSOD: manganese superoxide dismutase; IDH2: isocitrate dehydrogenase; Forkhead box O 3a (FOXO3a); LCAD: longchain acyl-CoA dehydrogenase; AMPK: AMP-activated protein kinase; GSH-Px: glutathione peroxidase; PGC-1α: peroxisome proliferator-activated receptor gamma coactivator 1-alpha; ERRα: estrogen-related receptor alpha; NRF1: nuclear respiratory factor 1; TFAM: transcription factor A, mitochondrial; OGG1: 8-oxoguanine glycosylase; MFN-1: mitofusin-1; OPA1: dynamin-like 120 kDa protein; Ku70; ATP-dependent DNA helicase II, 70 kDa subunit; BCL-2: B-cell lymphoma 2; NF-κB: nuclear factor kappa-light-chain enhancer of activated B cells; TF: transcription factor. Gene Expression and Regulation in Mammalian Cells -Transcription Toward the Establishment of Novel Therapeuticsmouse hearts of myocardial infarction and decrease the associated damage [103].…”

Section: Changes In Sirtuin 3 Expression In Carcinogenesismentioning

confidence: 99%

“…Investigators report that SIRT3 regulates the activity of the transcription factors, Forkhead box O 3a (FOXO3a), and nuclear factor κB (NF-κB) [24,25]; however, regulation of SIRT3 transcription itself is not completely understood up-to-date. SIRT3 gene is located in a bidirectional arrangement with another gene, called PSMD13, in a phylogenetically conserved manner.…”

Section: Introductionmentioning

confidence: 99%

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Changes in the Expression and the Role of Sirtuin 3 in Cancer Cells and in Cardiovascular Health and Disease

Özden¹,

Tural²

2018

Gene Expression and Regulation in Mammalian Cells - Transcription Toward the Establishment of Novel Therapeutics

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Sirtuin 3, an NAD + -dependent deacetylase, whose expression is considered a marker in life extension, is downregulated with age and in various diseases. Sirtuin 3 is predominantly localized to the mitochondria and considered a fidelity protein for the integrity and function of this organelle. Some studies report its localization in the nucleus to regulate the expression of stress response-related genes and that reduced expression of SIRT3 produces a cellular milieu permissive for human pathologies. Since the expression and activity of Sirtuin 3 are important for the regulation of antioxidant defense, metabolism, and apoptosis initiation, the expression of SIRT3 is also important in the context of ageassociated illnesses. A variety of small molecules are being developed to modulate the expression or activity of Sirtuin 3 and are potentially a valuable strategy to change mitochondrial acetylome to treat several diseases. The AMPK-PGC1α-SIRT3 axis plays a critical role in preserving mitochondrial biogenesis and function. Here, we summarize how changes in Sirtuin 3 expression are regulated in cancer and dysfunctions in cardiovascular diseases. The potential therapeutic strategies by targeting Sirtuin 3 expression to improve mitochondrial function in cancer and cardiovascular diseases are summarized.

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Section: Changes In Sirtuin 3 Expression In Carcinogenesismentioning

confidence: 99%

Section: Changes In Sirtuin 3 Expression In Carcinogenesismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Changes in the Expression and the Role of Sirtuin 3 in Cancer Cells and in Cardiovascular Health and Disease

Özden¹,

Tural²

2018

Gene Expression and Regulation in Mammalian Cells - Transcription Toward the Establishment of Novel Therapeutics

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“…They observed a reduction of apoptosis mediated by Bax which is hindered by Ku-70 binding, and confirmed that increased binding of Bax and Ku-70 is due to the deacetylation of Ku-70 by SIRT3. Chen et al (2013) pointed out that NF-κB represents another target of SIRT3, which is responsible for the survival of cardiomyocytes exposed to H 2 O 2 . They found that SIRT3 was down-regulated by oxidative stress in H9C2 cardiomyocytes and treatment with resveratrol reversed the stress-induced expression changes.…”

Section: Role Of Sirt3 In Attenuating Ischemia And/or Reperfusion-indmentioning

confidence: 99%

Roles of SIRT3 in heart failure: from bench to bedside

Liu

Song

et al. 2016

J. Zhejiang Univ. Sci. B

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Heart failure (HF) represents the most common endpoint of most cardiovascular diseases (CVDs) which are the leading causes of death around the world. Despite the advances in treating CVDs, the prevalence of HF continues to increase. It is believed that better results of prognosis are obtained from prevention rather than additional treatment for HF. Therefore, it is reasonable to prevent the development of CVDs or other complications to HF. Most types of HF are attributed to contractile dysfunction, cardiac hypertrophy or remodeling, and ischemic injuries. SIRT3 is a mitochondrial nicotinamide adenine dinucleotide (NAD + )-dependent deacetylase whose substrates vary from metabolic biogenesis-associated proteins to stress-responsive proteins. In recent years, a number of studies have highlighted the cardio-protective role of SIRT3 and, as such, efforts have been made to induce over-expression or increased activity of this protein. In this review, we provide an overview of the roles of SIRT3 in cardiac hypertrophy induced by pressure overload or agonists and cardiomyocytes ischemic injuries. Moreover, we will introduce the application of SIRT3 agonists in the prevention of cardiac hypertrophy and ischemia reperfusion injury.

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“…További fontos szabadgyök-hatásként említenénk, hogy gátolják a hiszton-deacetiláz-III, a SIRT1-3-deacetilázt, amelyeknek alapvető szerepe van az NF-κB/Bcl-2/Bax jelátvitel út leszabályozásában [21].…”

Section: A Ros Következményei Szívelégtelenségbenunclassified

Az oxidatív stressz szerepe szívelégtelenségben

Gal

Halmosi

2015

Orvosi Hetilap

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Az oxidatív stressz fontos szerepet játszik a szívelégtelenség kialakulásában. A szívizomzatban megtalálható összes sejttípus részt vesz az oxigén-és a nitrogén-szabadgyökök termelésében. A reaktívoxigén-származékok potenciális forrásának a szívben a NADPH-oxidáz, a nitrogén-oxid-szintázok, a lipoxigenázok, a ciklooxigenázok, a xantinoxidáz, a citokróm P450 enzimek, illetve a mitokondriális légzési lánc elemei tekinthetők. A reaktívoxigén-származékok okozta károsodás magában foglalja mind a vascularis rendszer (endotheldiszfunkció, atherosclerosis), mind a myocardium direkt károsodását (bal kamrai remodelling). A reaktívoxigén-származékok sejtszinten fehérje-, lipid-és DNSkárosodáshoz, valamint számos jelátviteli út modifi kációjához vezetnek, amelyek központi szerepet töltenek be a remodelling, a hypertrophia és a kamrai dilatatio kialakulásában. Orv. Hetil., 2015, 156(47), 1916-1920 Kulcsszavak: oxidatív stressz, reaktívoxigén-származékok, remodelling, szívelégtelenség The role of oxidative stress in heart failureOxidative stress plays an important role in the development of heart failure. Reactive oxygen and nitrogen species can be generated in all cell types that can be found in the myocardium. Potential sources of reactive oxygen species are the NADPH oxidases, nitric oxide synthase, lipoxygenases, cyclooxygenase, xanthine oxidase, cytochrome P450 enzymes, and the mitochondrial respiratory chain. The reactive oxygen species mediated damages are implicated in both the vascular system (endothelial dysfunction, atherosclerosis) and the myocardium (remodeling). Oixidative stress causes lipid and protein oixidation as well as single stranded DNA breaks and induces changes in signaling pathways which serve as central transducers of cardiac hypertrophic growth, remodeling and/or ventricular dilatation.Keywords: oxidative stress, reactive oxygen species, remodeling, heart failure Gál, R., Halmosi, R. [The role of oxidative stress in heart failure]. Orv. Hetil., 2015Hetil., , 156(47), 1916Hetil., -1920 Rövidítések Akt-1/GSK-3β = glikogénszintáz-kináz-3β; CaMKII = kalcium-kalmodulin-kináz II; COX = ciklooxigenáz; eNOS = endothelialis NOS; ERK 1/2 = extracellular signal-regulated protein kinase 1/2; ESR = elektronspin-rezonancia; JNK = c-Jun NH2-terminális kináz; NO = nitrogén-monoxid; NOS = nitrogén-oxid-szintáz; p38-MAPK = p38 mitogénaktivált fehérje kináz; PARP-1 = poli(ADP-ribóz) polimeráz-1; PKC = pro teinkináz C; ROS = (reactive oxygen species) reaktívoxi-gén-származékok Az oxidatív stressz a reaktívoxigén-vagy nitrogénerede-tű szabad gyökök keletkezése és az antioxidáns védő-rendszerek közötti egyensúly megbomlása, a sejtek oxidoredukciós állapotának megváltozása során lép fel, amikor a redoxállapot az oxidáció irányába tolódik el. Az oxidatív stressz következtében a sejtek szinte mindegyik biomolekulája sérülhet [1]. Nem meglepő ezért, hogy a szabad gyökös károsodások fontos patogenetikai ténye-zők a legtöbb betegség kialakulásában. Így van ez a szív-ér rendszeri betegségek és a szívelégtelenség esetén is.A ...

show abstract

SIRT3 protects cardiomyocytes from oxidative stress-mediated cell death by activating NF-κB

Cited by 112 publications

References 22 publications

Changes in the Expression and the Role of Sirtuin 3 in Cancer Cells and in Cardiovascular Health and Disease

Changes in the Expression and the Role of Sirtuin 3 in Cancer Cells and in Cardiovascular Health and Disease

Roles of SIRT3 in heart failure: from bench to bedside

Az oxidatív stressz szerepe szívelégtelenségben

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