Erratum to: Resveratrol increases AdipoR1 and AdipoR2 expression in type 2 diabetic nephropathy

Park, Hoon Suk; Lim, Ji Hee; Kim, Min Young; Kim, Yaeni; Hong, You Ah; Choi, Sun Ryoung; Chung, Sungjin; Kim, Hyung Wook; Choi, Bum Soon; Kim, Yong Soo; Chang, Yoon Sik; Park, Cheol Whee

doi:10.1186/s12967-016-0967-9

Cited by 6 publications

(6 citation statements)

References 1 publication

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“…Notably, amount of evidence has proved that SIRT1 cooperates with AMPK to enhance the ability of PGC-1a to attenuate endothelial dysfunction via stimulating mitochondrial biogenesis (53) and activating gluconeogenic fatty acid oxidation genes (54,55). In addition, SIRT1-AMPK-PGC-1a pathway exerts its anti-oxidative activity in other diabetic vascular complications including brain complications (56), diabetic cardiomyopathy, and diabetic nephropathy (57,58). Furthermore, PGC-1a can be directly activated by SIRT1 without AMPK to ease metabolic disorders in high glucoseinduced endothelial oxidative damage (59) and Drp-mediated mitochondrial fission in diabetic hearts (60).…”

Section: Inhibition Of Oxidative Stress By Sirt1-ampk-pgc-1amentioning

confidence: 99%

“…It has been proved that expression of PPARa was reduced by hyperglycemia, and SIRT1 activated PPARa pathway to reduce ROS in diabetic vascular diseases (73,74). In addition, AMPK-SIRT1-PPARa was activated by resveratrol to alleviate oxidative stress and endothelial dysfunction in type 2 diabetic nephropathy (58). However, unlike FOXOs, PPARa is not a directly target deacetylated by SIRT1, but its activity can be enhanced by SIRT1 indirectly through the coactivators, such as AMPK and PGC-1a (75,76).…”

Section: Inhibition Of Oxidative Stress By Sirt1-ampk-pparamentioning

confidence: 99%

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SIRT1 Antagonizes Oxidative Stress in Diabetic Vascular Complication

2020

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Diabetic mellitus (DM) is a significant public health concern worldwide with an increased incidence of morbidity and mortality, which is particularly due to the diabetic vascular complications. Several pivotal underlying mechanisms are associated with vascular complications, including hyperglycemia, mitochondrial dysfunction, inflammation, and most importantly, oxidative stress. Oxidative stress triggers defective angiogenesis, activates pro-inflammatory pathways and causes long-lasting epigenetic changes to facilitate the development of vascular complications. Therefore, therapeutic interventions targeting oxidative stress are promising to manage diabetic vascular complications. Sirtuin1 (SIRT1), a class III histone deacetylase belonging to the sirtuin family, plays critical roles in regulating metabolism and ageing-related pathological conditions, such as vascular diseases. Growing evidence has indicated that SIRT1 acts as a sensing regulator in response to oxidative stress and attenuates vascular dysfunction via cooperating with adenosine-monophosphate-activated protein kinase (AMPK) to activate antioxidant signals through various downstream effectors, including peroxisome proliferator-activated receptor-gamma co-activator 1 (PGC-1α), forkhead transcription factors (FOXOs), and peroxisome proliferative-activated receptor α (PPARα). In addition, SIRT1 interacts with hydrogen sulfide (H2S), regulates NADPH oxidase, endothelial NO synthase, and mechanistic target of rapamycin (mTOR) to suppress oxidative stress. Furthermore, mRNA expression of sirt1 is affected by microRNAs in DM. In the current review, we summarize recent advances illustrating the importance of SIRT1 in antagonizing oxidative stress. We also discuss whether modulation of SIRT1 can serve as a therapeutic strategy to treat diabetic vascular complications.

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Section: Inhibition Of Oxidative Stress By Sirt1-ampk-pgc-1amentioning

confidence: 99%

Section: Inhibition Of Oxidative Stress By Sirt1-ampk-pparamentioning

confidence: 99%

SIRT1 Antagonizes Oxidative Stress in Diabetic Vascular Complication

2020

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“…Basic studies show that PPARα/γ dual receptor agonists (tesaglitazar) can increase serum APN levels to suppress T2DM [79]. Resveratrol prevents diabetic nephropathy via the following mechanism: resveratrol activates the AMPK-SIRT1-PGC-1alpha axis and PPARα by increasing AdipoR1 and AdipoR2 expression and prevents high glucose-induced oxidative stress and cell apoptosis [80]. Additionally, AdipoRon directly activates intrarenal AdipoR1 and AdipoR2 and promotes downstream reactions, thereby restrainting renal fibrosis; this effect is unrelated to the systemic effect of APN.…”

Section: Adiponectin-associated Renal Fibrosis Treatmentmentioning

confidence: 99%

Adiponectin in renal fibrosis

Jing

Tang

Shi

et al. 2020

Aging

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Renal fibrosis is an inevitable consequence of parenchymal scarring and is the common final pathway that mediates almost all progressive renal diseases. Adiponectin, a hormone produced by adipose tissue, possesses potent anti-insulin, anti-inflammatory, and anti-fibrotic properties. Reportedly, adiponectin serves as an important messenger that facilitates complex interactions between adipose tissue and other metabolically related organs. In recent years, a growing body of evidence supports adiponectin involvement in renal fibrosis. These studies provide a deeper understanding of the molecular mechanism of action of adiponectin in renal fibrosis and also offer a potential preventive and therapeutic target for renal fibrosis. In this review, the physiological role of adiponectin is briefly introduced, and then the mechanism of adiponectin-mediated renal fibrosis and the related signaling pathways are described. Finally, we summarize the findings regarding the clinical value of adiponectin in renal fibrotic diseases and prospected its application potential.

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“…Resveratrol does inhibit obesity at pharmacological concentrations, prevent heightened hyperinsulinemia, or inhibit mTOR in vitro and therefore did not inhibit cellular senescence like rapamycin does [11]. Large levels of resveratrol have recently been shown to induce autophagy when inhibiting mTOR directly through ATP competition [78]. Combination therapy of rapamycin and resveratrol has proven synergistic in treatment of breast cancer cells [79,80].…”

Section: Autophagymentioning

confidence: 99%

“…Rapamycin is a much larger macrocycle molecule (MW = 914) with both hydrogen donor and acceptor moieties compared to the smaller resveratrol (MW = 228) and rapamycin (MW = 129) (Figure 4). Future docking, crystallography, and NMR studies would be interesting to determine if other molecules could mimic ATP, directly binding to the ATP pocket on mTOR as it has been suggested resveratrol does [78]. A structural mimic of ATP acting as an antagonist can seem conceptually attractive and likely have broad effects on multiple energy sensing proteins, but would also likely have lower than desired specificity.…”

Section: Preclinical and Clinical Studiesmentioning

confidence: 99%

Where and How in the mTOR Pathway Inhibitors Fight Aging: Rapamycin, Resveratrol, and Metformin

Arbor¹

2019

Resveratrol - Adding Life to Years, Not Adding Years to Life

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The molecular mechanisms underlying the quality and quantity of life extension appear to sometimes be orthogonal. For example, while resveratrol has continued to prove beneficial in reducing obesity, it has had less efficacy in extending lifespan. On the other hand, rapamycin and the chemically similar rapalogs extend lifespan across genera of life from yeast, to nematodes, to mice. Caloric restriction (CR) and bioavailable small molecules, which mimic a fasted state, upregulate autophagy, catabolism of fats over anabolism of carbohydrates, and decrease oxidative stress and inflammation. CR mimics are currently being investigated to elucidate the best dosage, route of administration, timing in life, where best to inhibit in the mTOR pathway, and effects of long-term use on mTORC1 verse mTORC2 complexes. Comparisons between rapamycin, resveratrol, and metformin targets, downstream pathway effects, dosage, and clinical trials will be discussed.

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Erratum to: Resveratrol increases AdipoR1 and AdipoR2 expression in type 2 diabetic nephropathy

Cited by 6 publications

References 1 publication

SIRT1 Antagonizes Oxidative Stress in Diabetic Vascular Complication

SIRT1 Antagonizes Oxidative Stress in Diabetic Vascular Complication

Adiponectin in renal fibrosis

Where and How in the mTOR Pathway Inhibitors Fight Aging: Rapamycin, Resveratrol, and Metformin

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