TXNIP is a Mediator of ER Stress-Induced β-Cell Inflammation and Apoptosis: A Dissertation

摘要: Diabetes mellitus is a group of metabolic disorders characterized by hyperglycemia. The pathogenesis these diseases involves β-cell dysfunction and death. primary function β-cells to tightly regulate the secretion, production, storage insulin in response blood glucose levels. In order manage biosynthesis, have an elaborate endoplasmic reticulum (ER). ER essential organelle for proper processing folding proteins such as proinsulin. Proteins fold properly when protein load balances with capacity that handles this load. Disruption homeostasis genetic environmental stimuli leads accumulation misfolded unfolded proteins, condition known stress. Upon stress, (UPR) activated. UPR signaling network aims alleviate stress restore promoting cell survival. Hence, allows handle physiological fluctuations demand. However upon severe unresolvable conditions during diabetes progression, switches pathological outputs leading apoptosis. Severe may also trigger inflammation accumulating evidence suggests contributes failure, but mechanisms remain elusive. dissertation, we demonstrate thioredoxin interacting (TXNIP) mediates induced During DNA microarray analysis identify novel survival death components UPR, identified