@article{shrestha_pathological_2021,
	title = {Pathological β-Cell Endoplasmic Reticulum Stress in Type 2 Diabetes: Current Evidence},
	volume = {12},
	issn = {1664-2392},
	url = {https://www.frontiersin.org/articles/10.3389/fendo.2021.650158/full},
	doi = {10.3389/fendo.2021.650158},
	shorttitle = {Pathological β-Cell Endoplasmic Reticulum Stress in Type 2 Diabetes},
	abstract = {The notion that in diabetes pancreatic β-cells express endoplasmic reticulum ({ER}) stress markers indicative of increased unfolded protein response ({UPR}) signaling is no longer in doubt. However, what remains controversial is whether this increase in {ER} stress response actually contributes importantly to the β-cell failure of type 2 diabetes (akin to ‘terminal {UPR}’), or whether it represents a coping mechanism that represents the best attempt of β-cells to adapt to changes in metabolic demands as presented by disease progression. Here an intercontinental group of experts review evidence for the role of {ER} stress in monogenic and type 2 diabetes in an attempt to reconcile these disparate views. Current evidence implies that pancreatic β-cells require a regulated {UPR} for their development, function and survival, as well as to maintain cellular homeostasis in response to protein misfolding stress. Prolonged {ER} stress signaling, however, can be detrimental to β-cells, highlighting the importance of “optimal” {UPR} for {ER} homeostasis, β-cell function and survival.},
	pages = {650158},
	journaltitle = {Frontiers in Endocrinology},
	shortjournal = {Front. Endocrinol.},
	author = {Shrestha, Neha and De Franco, Elisa and Arvan, Peter and Cnop, Miriam},
	urldate = {2021-09-07},
	date = {2021-04-22},
	keywords = {{WP}5},
}