Molecular aspects of pancreatic beta-cell dysfunction: Oxidative stress, microRNA, and long noncoding RNA


Por: Saeedi Borujeni MJ, Esfandiary E, Baradaran A, Valiani A, Ghanadian M, Codoñer-Franch P, Basirat R, Alonso-Iglesias E, Mirzaei H and Yazdani A

Publicada: 1 jun 2019
Resumen:
Metabolic syndrome is known as a frequent precursor of type 2 diabetes mellitus (T2D). This disease could affect 8% of the people worldwide. Given that pancreatic beta-cell dysfunction and loss have central roles in the initiation and progression of the disease, the understanding of cellular and molecular pathways associated with pancreatic beta-cell dysfunction can provide more information about the underlying pathways involved in T2D. Multiple lines evidence indicated that oxidative stress, microRNA, and long noncoding RNA play significant roles in various steps of diseases. Oxidative stress is one of the important factors involved in T2D pathogenesis. This could affect the function and survival of the beta cell via activation or inhibition of several processes and targets, such as receptor-signal transduction, enzyme activity, gene expression, ion channel transport, and apoptosis. Besides oxidative stress, microRNAs and noncoding RNAs have emerged as epigenetic regulators that could affect pancreatic beta-cell dysfunction. These molecules exert their effects via targeting a variety of cellular and molecular pathways involved in T2D pathogenesis. Here, we summarized the molecular aspects of pancreatic beta-cell dysfunction. Moreover, we highlighted the roles of oxidative stress, microRNAs, and noncoding RNAs in pancreatic beta-cell dysfunction.

Filiaciones:
Saeedi Borujeni MJ:
 Department of Anatomical SCIENCES and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Esfandiary E:
 Department of Anatomical SCIENCES and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Baradaran A:
 Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Valiani A:
 Department of Anatomical SCIENCES and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Ghanadian M:
 Department of Pharmacognosy, Faculty of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran

:
 Department of Pediatrics, Obstetrics and Gynecology, University of Valencia, Valencia, Spain

Basirat R:
 Department of Clinical Nutrition, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Shiraz, Iran

Alonso-Iglesias E:
 Department of Biochemistry and Molecular Biology, University of Valencia, Valencia, Spain

Mirzaei H:
 Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran

Yazdani A:
 School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
ISSN: 10974652





JOURNAL OF CELLULAR PHYSIOLOGY
Editorial
John Wiley & Sons Inc., 111 RIVER ST, HOBOKEN 07030-5774, NJ USA, Estados Unidos America
Tipo de documento: Review
Volumen: 234 Número: 6
Páginas: 8411-8425
WOS Id: 000459314500064
ID de PubMed: 30565679

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