1,25-Dihydroxyvitamin-D3 prevents the development of diabetic cardiomyopathy in type 1 diabetic rats by enhancing autophagy via inhibiting the β-catenin/TCF4/GSK-3β/mTOR pathway

Wei, Huijie; Qu, Hua; Wang, Hang; Ji, Baolan; Ding, Yao; Liú, Dan; Duan, Yang; Liang, Huimin; Peng, Chuan; Xiao, Xiaoqiu; Deng, Hongkui

doi:10.1016/j.jsbmb.2017.02.007

Cited by 57 publications

(35 citation statements)

References 46 publications

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“…; Wei et al . ). It is possible that vitamin D will act to promote autophagy by regulating the level of Ca 2+ through its ability to promote the expression of Ca 2+ pumps and Ca 2+ buffers as will be described in a later section.…”

Section: Introductionmentioning

confidence: 97%

Vitamin D deficiency accelerates ageing and age‐related diseases: a novel hypothesis

Berridge

2017

The Journal of Physiology

117

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Ageing can occur at different rates, but what controls this variable rate is unknown. Here I have developed a hypothesis that vitamin D may act to control the rate of ageing. The basis of this hypothesis emerged from studyng the various cellular processes that control ageing. These processes such as autophagy, mitochondrial dysfunction, inflammation, oxidative stress, epigenetic changes, DNA disorders and alterations in Ca and reactive oxygen species (ROS) signalling are all known to be regulated by vitamin D. The activity of these processes will be enhanced in individuals that are deficient in vitamin D. Not only will this increase the rate of ageing, but it will also increase the probability of developing age-related diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis and cardiovascular disease. In individual with normal vitamin D levels, these ageing-related processes will occur at lower rates resulting in a reduced rate of ageing and enhanced protection against these age-related diseases.

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Section: Introductionmentioning

confidence: 97%

Vitamin D deficiency accelerates ageing and age‐related diseases: a novel hypothesis

Berridge

2017

The Journal of Physiology

117

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“…Diabetic cardiomyopathy (DCM) is the primary cause of overt heart failure and death in diabetic individuals and affects nearly 12% of diabetic patients . Ma et al recently report that the heart failure rate in patients with diabetes is four times that in people without diabetes .…”

Section: Introductionmentioning

confidence: 99%

Gypenosides improve diabetic cardiomyopathy by inhibiting ROS‐mediated NLRP3 inflammasome activation

Zhang

Chen

Zong

et al. 2018

J Cellular Molecular Medi

107

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NLRP3 inflammasome activation plays an important role in diabetic cardiomyopathy (DCM), which may relate to excessive production of reactive oxygen species (ROS). Gypenosides (Gps), the major ingredients of Gynostemma pentaphylla (Thunb.) Makino, have exerted the properties of anti‐hyperglycaemia and anti‐inflammation, but whether Gps improve myocardial damage and the mechanism remains unclear. Here, we found that high glucose (HG) induced myocardial damage by activating the NLRP3 inflammasome and then promoting IL‐1β and IL‐18 secretion in H9C2 cells and NRVMs. Meanwhile, HG elevated the production of ROS, which was vital to NLRP3 inflammasome activation. Moreover, the ROS activated the NLRP3 inflammasome mainly by cytochrome c influx into the cytoplasm and binding to NLRP3. Inhibition of ROS and cytochrome c dramatically down‐regulated NLRP3 inflammasome activation and improved the cardiomyocyte damage induced by HG, which was also detected in cells treated by Gps. Furthermore, Gps also reduced the levels of the C‐reactive proteins (CRPs), IL‐1β and IL‐18, inhibited NLRP3 inflammasome activation and consequently improved myocardial damage in vivo. These findings provide a mechanism that ROS induced by HG activates the NLRP3 inflammasome by cytochrome c binding to NLRP3 and that Gps may be potential and effective drugs for DCM via the inhibition of ROS‐mediated NLRP3 inflammasome activation.

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“…Although cardiomyopathy and HF have been described in type 1 diabetes mellitus (DM) (Lind et al, 2011;Wei et al, 2017), the underlying pathophysiological mechanisms when HF and type 1 diabetes coexist remains unclear.…”

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confidence: 99%

The protective effect of kaempferol on heart via the regulation of Nrf2, NF‐κβ, and PI3K/Akt/GSK‐3β signaling pathways in isoproterenol‐induced heart failure in diabetic rats

Zhang

Guo

Wang

et al. 2019

Drug Development Research

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This study was designed to delineate the effect of kaempferol (KF) on heart failure (HF) in diabetic rats. Streptozotocin‐induced male diabetic rats received KF orally at 10 and 20 mg/kg for 42 consecutive days. In last 2 days of the experimental period, isoproterenol was subcutaneously injected at 85 mg/kg to induce HF. The hearts were processed for hemodynamic, biochemical, molecular, and histological investigations. Systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure were elevated in KF‐treated HF‐induced diabetic rats. Moreover, KF treatment resulted in decreased fasting blood glucose and glycosylated hemoglobin levels with increased serum insulin levels. Besides, serum cardiac injury markers like troponin‐I, creatine kinase‐muscle/brain, lactate dehydrogenase, and brain natriuretic peptide levels were significantly reduced in KF treatment. KF treatment has shown decrease in cardiac heme oxygenase‐1, nuclear factor erythroid 2–related factor 2 (Nrf‐2), and γ‐glutamylcysteine synthetase with increased Keap1 mRNA levels. The cardioprotection of KF was improved by inhibition of apoptosis via blocking phosphorylation of Akt/glycogen synthase kinase (GSK)‐3β and p38 mitogen‐activated protein‐kinase/extracellular signal‐regulated kinases signaling pathways in HF‐induced diabetic rats. Moreover, reduced cardiac apoptosis in KF treatment was confirmed by decreased terminal deoxynucleotidyl transferase dUTP nick‐end labeling (TUNEL) positive cells, histopathological changes in HF‐induced diabetic rats. Therefore, the cardioprotective effect of KF is attributed to the regulation of Nrf2, nuclear factor kappa‐light‐chain‐enhancer of activated B cells, and Akt/GSK‐3β signaling pathways in HF‐induced diabetic rats.

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1,25-Dihydroxyvitamin-D3 prevents the development of diabetic cardiomyopathy in type 1 diabetic rats by enhancing autophagy via inhibiting the β-catenin/TCF4/GSK-3β/mTOR pathway

Cited by 57 publications

References 46 publications

Vitamin D deficiency accelerates ageing and age‐related diseases: a novel hypothesis

Vitamin D deficiency accelerates ageing and age‐related diseases: a novel hypothesis

Gypenosides improve diabetic cardiomyopathy by inhibiting ROS‐mediated NLRP3 inflammasome activation

The protective effect of kaempferol on heart via the regulation of Nrf2, NF‐κβ, and PI3K/Akt/GSK‐3β signaling pathways in isoproterenol‐induced heart failure in diabetic rats

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