About: Inhibition of Miro1 disturbs mitophagy and pancreatic β-cell function interfering insulin release via IRS-Akt-Foxo1 in diabetes

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About: Inhibition of Miro1 disturbs mitophagy and pancreatic β-cell function interfering insulin release via IRS-Akt-Foxo1 in diabetes Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Inhibition of Miro1 disturbs mitophagy and pancreatic β-cell function interfering insulin release via IRS-Akt-Foxo1 in diabetes
Creator	Yang, Yibin Liu, Chunyan Chen, Lingling Gao, Jianfeng Men, Xiuli Sun, Jiazhong Wei, Yongchang Xie, Zhiwen Yang, Sijun Zhou, Fuling Chan, Lawrence Keating, Damien
Source	PMC
abstract	Mitochondrial function is essential to meet metabolic demand of pancreatic beta cells respond to high nutrient stress. Mitophagy is an essential component to normal pancreatic β-cell function and has been associated with β-cell failure in Type 2 diabetes (T2D). Our previous studies have indicated that mitochondrial Rho (Miro) GTPase-mediated mitochondrial dysfunction under high nutrient stress leads to NOD-like receptor 3 (NLRP3)-dependent proinflammatory responses and subsequent insulin resistance. However, the in vivo mechanism by which Miro1 underlies mitophagy has not been identified. Here we show firstly that the expression of Miro is reduced in human T2D and mouse db/db islets and in INS-1 cell line exposed to high glucose and palmitate. β-cell specific ablation of Miro1 (Miro1f/f: Rip-cre mice, or (IKO) under high nutrient stress promotes the development of hyperglycemia. β-cells from IKO mice display an inhibition of mitophagy under oxidative stress and induces mitochondrial dysfunction. Dysfunctional mitophagy in IKO mice is represented by damaged islet beta cell mitochondrial and secretory capacity, unbalanced downstream MKK-JNK signalling without affecting the levels of MEK, ERK or p38 activation and subsequently, impaired insulin secretion signaling via inhibition IRS-AKT-Foxo1 pathway, leading to worsening glucose tolerance in these mice. Thus, these data suggest that Miro1 may be responsible for mitophagy deficiency and β-cell dysfunction in T2D and that strategies target Miro1 in vivo may provide a therapeutic target to enhance β-cell mitochondrial quality and insulin secretion to ameliorate complications associated with T2D.
has issue date	2017-09-16(xsd:dateTime)
bibo:doi	10.18632/oncotarget.20963
bibo:pmid	29207597
has license	cc-by
sha1sum (hex)	f5fb59693963a0b96d112341f8f2a9f2b1d7a34c
schema:url	https://doi.org/10.18632/oncotarget.20963
resource representing a document's title	Inhibition of Miro1 disturbs mitophagy and pancreatic β-cell function interfering insulin release via IRS-Akt-Foxo1 in diabetes
has PubMed Central identifier	PMC5710878
has PubMed identifier	29207597
schema:publication	Oncotarget
resource representing a document's body	covid:f5fb59693963a0b96d112341f8f2a9f2b1d7a34c#body_text
is schema:about of	named entity 'FOXO1' named entity 'INS' named entity 'nutrient' named entity 'respond' named entity 'nutrient' named entity 'β-cell' named entity 'target' named entity 'β-cell' named entity 'high' named entity 'Our' named entity 'MITOPHAGY' named entity 'AKT' named entity 'INHIBITION' named entity 'HAVE' named entity 'MAY BE' named entity 'DEFICIENCY' named entity 'CAPACITY' named entity 'REDUCED' named entity 'IMPAIRED INSULIN SECRETION' named entity 'MEK' named entity 'MIRO1' named entity 'NORMAL' named entity 'MICE' named entity 'FIRSTLY' named entity 'COMPLICATIONS' named entity 'INSULIN SECRETION' named entity 'COMPONENT' named entity 'PANCREATIC' named entity 'ESSENTIAL' named entity 'ISLET BETA CELL' named entity 'DISPLAY' named entity 'MITOCHONDRIAL QUALITY' named entity 'DOWNSTREAM' named entity 'ACTIVATION' named entity 'EXPRESSION' named entity 'GLUCOSE TOLERANCE' named entity 'SIGNALING' named entity 'T2D' named entity 'HERE' named entity 'DYSFUNCTIONAL' named entity 'CELLS' named entity 'ASSOCIATED WITH' named entity 'CRE' named entity 'RIP' named entity 'TARGET' named entity 'MITOCHONDRIAL FUNCTION' named entity 'MECHANISM' named entity 'OUR' named entity 'PALMITATE' named entity 'THERAPEUTIC TARGET' named entity 'RECEPTOR' named entity 'FAILURE' named entity 'HUMAN' named entity 'INS-1 CELL' named entity 'RHO' named entity 'IDENTIFIED' named entity 'THESE' named entity 'SIGNALLING' named entity 'LEADING' named entity 'AKT' named entity 'SUBSEQUENT' named entity 'PATHWAY' named entity 'LEADS' named entity 'NUTRIENT STRESS' named entity 'LEVELS' named entity 'PREVIOUS' named entity 'HIGH' named entity 'DEMAND' named entity 'MIRO' named entity 'PANCREATIC BETA CELLS'

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