296-LB: Loss of SERCA2 Induces Mitochondrial Dysfunction, Increases ß-Cell Senescence, and Accelerates Type 1 Diabetes Development

Type 1 diabetes (T1D) results from immune-mediated destruction of pancreatic β-cells. Senescence and activation of a senescence-associated secretory phenotype (SASP) in β-cells may contribute to T1D pathogenesis; however, the mechanisms responsible for this phenotype are not well understood. We hypo...

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Veröffentlicht in:	Diabetes (New York, N.Y.) N.Y.), 2023-06, Vol.72 (Supplement_1), p.1
Hauptverfasser:	WEAVER, STACI A., BONE, ROBERT N., ACRI, DOMINIC J., KIM, JUNGSU, KONO, TATSUYOSHI, DAHL, RUSSELL, EIZIRIK, DECIO L., SYED, FAROOQ, EVANS-MOLINA, CARMELLA
Format:	Artikel
Sprache:	eng
Schlagworte:	Age Allosteric properties ATP synthase Beta cells Ca2+-transporting ATPase Calcium (mitochondrial) Calcium (reticular) Cell activation Diabetes Diabetes mellitus (insulin dependent) Endoplasmic reticulum Insulitis Membrane potential Membrane proteins Mitochondria Oxygen consumption Phenotypes Senescence
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