Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah 67155-1616, Iran
Mona Sadeghalvad
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran 1416634793, Iran
Niloofar Yavari
Department of Cellular and Molecular Medicine, The Panum Institute, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark
Rosita Primavera
Interventional Regenerative Innovation at Stanford (IRIS), Department of Radiology, Stanford University School of Medicine, Palo Alto, CA 94304, USA
Setareh Soltani
Clinical Research Development Center, Taleghani and Imam Ali Hospital, Kermanshah University of Medical Sciences, Kermanshah 67145-1673, Iran
Shashank Chetty
Interventional Regenerative Innovation at Stanford (IRIS), Department of Radiology, Stanford University School of Medicine, Palo Alto, CA 94304, USA
Abantika Ganguly
Interventional Regenerative Innovation at Stanford (IRIS), Department of Radiology, Stanford University School of Medicine, Palo Alto, CA 94304, USA
Shobha Regmi
Interventional Regenerative Innovation at Stanford (IRIS), Department of Radiology, Stanford University School of Medicine, Palo Alto, CA 94304, USA
Tina Fløyel
Translational Type 1 Diabetes Research, Department of Clinical Research, Steno Diabetes Center Copenhagen, 2730 Herlev, Denmark
Simranjeet Kaur
Translational Type 1 Diabetes Research, Department of Clinical Research, Steno Diabetes Center Copenhagen, 2730 Herlev, Denmark
Aashiq H. Mirza
Translational Type 1 Diabetes Research, Department of Clinical Research, Steno Diabetes Center Copenhagen, 2730 Herlev, Denmark
Avnesh S. Thakor
Interventional Regenerative Innovation at Stanford (IRIS), Department of Radiology, Stanford University School of Medicine, Palo Alto, CA 94304, USA
Flemming Pociot
Translational Type 1 Diabetes Research, Department of Clinical Research, Steno Diabetes Center Copenhagen, 2730 Herlev, Denmark
Reza Yarani
Interventional Regenerative Innovation at Stanford (IRIS), Department of Radiology, Stanford University School of Medicine, Palo Alto, CA 94304, USA
Pancreatic β cells are central to glycemic regulation through insulin production. Studies show autophagy as an essential process in β cell function and fate. Autophagy is a catabolic cellular process that regulates cell homeostasis by recycling surplus or damaged cell components. Impaired autophagy results in β cell loss of function and apoptosis and, as a result, diabetes initiation and progress. It has been shown that in response to endoplasmic reticulum stress, inflammation, and high metabolic demands, autophagy affects β cell function, insulin synthesis, and secretion. This review highlights recent evidence regarding how autophagy can affect β cells’ fate in the pathogenesis of diabetes. Furthermore, we discuss the role of important intrinsic and extrinsic autophagy modulators, which can lead to β cell failure.
