miRNAs: novel regulators of autoimmunity-mediated pancreatic β-cell destruction in type 1 diabetes

Zheng, Ying; Wang, Zhen; Zhou, Zhiguang

doi:10.1038/cmi.2017.7

Cited by 59 publications

(36 citation statements)

References 114 publications

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“…Owing to their widespread distribution from prokaryotic to mammalian cells, it is not difficult to comprehend their extensive roles in maintaining cellular physiology and internal homeostasis [281]. With respect to the central nervous system, developmental researchers have identified that miRNAs are inevitable regulators during neurogenesis and maturity phase.…”

Section: Major Cancer-related Signaling Pathways With Links To Ad mentioning

confidence: 99%

Functional analyses of major cancer-related signaling pathways in Alzheimer's disease etiology

Guo

Cheng²,

North

2017

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Alzheimer’s disease (AD) is an aging-related neurodegenerative disease and accounts for majority of human dementia. The hyper-phosphorylated tau-mediated intracellular neurofibrillary tangle and amyloid β-mediated extracellular senile plaque are characterized as major pathological lesions of AD. Different from the dysregulated growth control and ample genetic mutations associated with human cancers, AD displays damage and death of brain neurons in the absence of genomic alterations. Although various biological processes predominately governing tumorigenesis such as inflammation, metabolic alteration, oxidative stress and insulin resistance have been associated with AD genesis, the mechanistic connection of these biological processes and signaling pathways including mTOR, MAPK, SIRT, HIF, and the FOXO pathway controlling aging and the pathological lesions of AD are not well recapitulated. Hence, we performed a thorough review by summarizing the physiological roles of these key cancer-related signaling pathways in AD pathogenesis, comprising of the crosstalk of these pathways with neurofibrillary tangle and senile plaque formation to impact AD phenotypes. Importantly, the pharmaceutical investigations of anti-aging and AD relevant medications have also been highlighted. In summary, in this review, we discuss the potential role that cancer-related signaling pathways may play in governing the pathogenesis of AD, as well as their potential as future targeted strategies to delay or prevent aging-related diseases and combating AD.

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Section: Major Cancer-related Signaling Pathways With Links To Ad mentioning

confidence: 99%

Functional analyses of major cancer-related signaling pathways in Alzheimer's disease etiology

Guo

Cheng²,

North

2017

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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“…Many experimental studies in cultured cells an d an imal models of T1DM have provided convincing evidence that miRNAs can participate in controlling β-cell fate, autoimmune damage of β-cells, an d regulation of insulin synthesis an d secretion [60]. In mice, the disruption of miR-155 promoted the onset of T1DM an d a reduction of Treg cell number [61].…”

Section: The Experimental Studies In Cultured Cells An D Animal Modelsmentioning

confidence: 99%

Epigenetic Regulation in Etiology of Type 1 Diabetes Mellitus

Černá

2019

IJMS

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Type 1 diabetes mellitus (T1DM) is caused by an autoimmune destruction of the pancreatic β-cells, a process in which autoreactive T cells play a pivotal role, and it is characterized by islet autoantibodies. Consequent hyperglycemia is requiring lifelong insulin replacement therapy. T1DM is caused by the interaction of multiple environmental and genetic factors. The integrations of environments and genes occur via epigenetic regulations of the genome, which allow adaptation of organism to changing life conditions by alternation of gene expression. T1DM has increased several-fold over the past half century. Such a short time indicates involvement of environment factors and excludes genetic changes. This review summarizes the most current knowledge of epigenetic changes in that process leading to autoimmune diabetes mellitus.

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“…The evidence at this moment suggests that the transition into PILs is under post-transcriptional control exerted by miRNAs (Figure 1 ). Interestingly, some miRNAs such as miR-375, miR-30d and miR-9, can control insulin synthesis and secretion by pancreatic beta-cells ( 85 ) in NOD mice. Whether miRNAs also regulate the intrathymic production of proinsulin/insulin and IGF remains unknown.…”

Section: The Role Of Mirnas Throughout Transition Of Thymocytes Into mentioning

confidence: 99%

Abnormal T-Cell Development in the Thymus of Non-obese Diabetic Mice: Possible Relationship With the Pathogenesis of Type 1 Autoimmune Diabetes

et al. 2018

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Type 1 diabetes (T1D) is an autoimmune disease caused by the destruction of insulin-producing cells in the pancreas, by direct interactions with autoreactive pancreas infiltrating T lymphocytes (PILs). One of the most important animal models for this disease is the non-obese diabetic (NOD) mouse. Alterations in the NOD mouse thymus during the pathogenesis of the disease have been reported. From the initial migratory disturbances to the accumulation of mature thymocytes, including regulatory Foxp3+ T cells, important mechanisms seem to regulate the repertoire of T cells that leave the thymus to settle in peripheral lymphoid organs. A significant modulation of the expression of extracellular matrix and soluble chemoattractant molecules, in addition to integrins and chemokine receptors, may contribute to the progressive accumulation of mature thymocytes and consequent formation of giant perivascular spaces (PVS) that are observed in the NOD mouse thymus. Comparative large-scale transcriptional expression and network analyses involving mRNAs and miRNAs of thymocytes, peripheral T CD3+ cells and PILs provided evidence that in PILs chemokine receptors and mRNAs are post-transcriptionally regulated by miR-202-3p resulting in decreased activity of these molecules during the onset of T1D in NOD mice. In this review, we discuss the abnormal T-cell development in NOD mice in the context of intrathymic expression of different migration-related molecules, peptides belonging to the family of insulin and insulin-like growth factors as well as the participation of miRNAs as post-transcriptional regulators and their possible influence on the onset of aggressive autoimmunity during the pathogenesis of T1D.

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miRNAs: novel regulators of autoimmunity-mediated pancreatic β-cell destruction in type 1 diabetes

Cited by 59 publications

References 114 publications

Functional analyses of major cancer-related signaling pathways in Alzheimer's disease etiology

Functional analyses of major cancer-related signaling pathways in Alzheimer's disease etiology

Epigenetic Regulation in Etiology of Type 1 Diabetes Mellitus

Abnormal T-Cell Development in the Thymus of Non-obese Diabetic Mice: Possible Relationship With the Pathogenesis of Type 1 Autoimmune Diabetes

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