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Abstract
Type 1 diabetes mellitus (T1DM) results from pancreatic β-cell failure to produce sufficient insulin, often due to β-cell destruction. This review examines T1DM pathophysiology, emphasizing the role of mitochondrial melatonin pathways in pancreatic β-cells, gut microbiome interactions, and bystander activation of memory CD8+ T cells. Mitochondrial melatonin suppression renders β-cells vulnerable to oxidative stress and dysfunctional mitophagy. Gut dysbiosis and permeability affect immune responses and mitochondrial function. The interplay between these factors contributes to β-cell apoptosis and autoimmune effects.
Publisher
International Journal of Molecular Sciences
Published On
Feb 07, 2023
Authors
Simona Santillo, Damiano, George Anderson
Tags
Type 1 diabetes mellitus
mitochondrial melatonin
gut microbiome
β-cell apoptosis
immune response
oxidative stress
autoimmunity

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