Pathophysiological significance of senescence marker protein‐30

Maruyama, Naoki; Ishigami, Akihito; Kondo, Yoshitaka

doi:10.1111/j.1447-0594.2010.00586.x

Cited by 41 publications

(47 citation statements)

References 41 publications

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“…SMP30 knockout mice show a short life with increased oxidant stress [36][37][38] and increased SA β-gal activity [39]. Therefore, to further confirm the anti-senescence function of PSPC, we performed double-immunofluorescence staining to analyze the expression of SMP30 in the vessel walls of mice in different groups.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Purple sweet potato color inhibits endothelial premature senescence by blocking the NLRP3 inflammasome

Sun

Fan

Wang

et al. 2015

The Journal of Nutritional Biochemistry

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Section: Accepted Manuscriptmentioning

confidence: 99%

Purple sweet potato color inhibits endothelial premature senescence by blocking the NLRP3 inflammasome

Sun

Fan

Wang

et al. 2015

The Journal of Nutritional Biochemistry

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“…160, 161 Misaka et al demonstrated that SMP30 is a marker of cardiac senescence as levels of this protein decrease in the murine myocardium with aging by as much as 40%. 162, 163 SMP30 has been shown to play a role in multi-organ senescence, including brain, lungs and kidneys.…”

Section: Novel Discoveries In Cardiac Agingmentioning

confidence: 99%

Heart Failure With Preserved Ejection Fraction

Loffredo

Nikolova

Pancoast

et al. 2014

Circulation Research

163

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Age-related diastolic dysfunction is a major factor in the epidemic of heart failure. In patients hospitalized with heart failure, diastolic heart failure is now as common as systolic heart failure. We now have many successful treatments for HFrEF, while specific treatment options for HFpEF patients remain elusive. The lack of treatments for HFpEF reflects our very incomplete understanding of this constellation of diseases. There are many pathophysiological factors in HFpEF, but aging appears to play an important role. Here we propose that aging of the myocardium is itself a specific pathophysiological process. New insights into the aging heart, including hormonal controls and specific molecular pathways such as microRNAs, are pointing to myocardial aging as a potentially reversible process. While the overall process of aging remains mysterious, understanding the molecular pathways of myocardial aging has never been more important. Unraveling these pathways could lead to new therapies for the enormous and growing problem of HFpEF.

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“…SMP30 is a novel 34-kDa protein whose expression in the liver, kidneys, and lungs decreases with age in an androgen-independent manner [6] [7]. Recently, SMP30 was verified as a gluconolactonase involved in L-ascorbic acid biosynthesis [8].…”

Section: Introductionmentioning

confidence: 99%

Ascorbic Acid Attenuates Acute Ethanol-Induced Liver Injury in SMP30 Knockout Mice

Cho¹,

Ullah²,

Elfadl³

et al. 2017

FNS

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Ascorbic acid (AA) is recognized as a free radical scavenger that protects cells from oxidative stress-induced damage. However, no studies have investigated the role of AA in acute alcoholic liver disease using senescence marker protein-30 (SMP30) knockout (KO) mice. SMP30 is a novel 34-kDa protein involved in AA biosynthesis. The present study aimed to elucidate the physiological functions of AA in acute ethanol-induced liver injury using SMP30 KO mice, which cannot synthesize AA in vivo. After a 4-week experimental period, mice were divided into six groups. The following three groups comprised the ethanol treatment groups: WT-E group (wild-type), KV-E group (AA-supplemented), and KT-E group (AA-deficient). Mice were exposed to an acute dose of ethanol (6 g ethanol/kg) administered by gavage once a day for three days. The other three control groups, namely, WT-C, KV-C, and KT-C control groups, received an equal volume of water via oral administration. Analysis of changes in body weight showed that mice in the KT-E group had significant loss of body weight compared to the control, KV-E, and WT-E groups. Behavioral analysis revealed that alcohol exposure significantly increased alcohol sensitivity in the KT-E group, whereas the WT-E, KV-E, and control groups developed ethanol tolerance. Aspartate transaminase (AST) levels in the KT-E group were significantly higher than those in the control, KV-E, and WT-E groups. The number of large and binucleated hepatocytes was significantly higher in the KT-E group than in the KV-E and WT-E groups. In addition, cytochrome P450 2E1 (CYP2E1) was over expressed in the central vein in the KT-E group when compared to the KV-E and WT-E groups. Our current findings indicate that AA supplementation in SMP30 KO mice can alleviate alcohol-induced liver damage by down regulating CYP2E1 expression. These results suggest that reduced CYP2E1 expression is a novel How to cite this paper:

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Pathophysiological significance of senescence marker protein‐30

Cited by 41 publications

References 41 publications

Purple sweet potato color inhibits endothelial premature senescence by blocking the NLRP3 inflammasome

Purple sweet potato color inhibits endothelial premature senescence by blocking the NLRP3 inflammasome

Heart Failure With Preserved Ejection Fraction

Ascorbic Acid Attenuates Acute Ethanol-Induced Liver Injury in SMP30 Knockout Mice

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