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Interaction between mitochondria and the endoplasmic reticulum: implications for the pathogenesis of type 2 diabetes mellitus.

Leem J, Koh EH - Exp Diabetes Res (2011)

Bottom Line: It is now well established that ER stress causes apoptotic cell death by disturbing mitochondrial Ca(2+) homeostasis.In addition, recent studies have shown that mitochondrial dysfunction causes ER stress.Structural and functional communications between mitochondria and the ER are also discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, University of Ulsan College of Medicine, 388-1 Poongnap-Dong, Songpa-Gu, Seoul 138-736, Republic of Korea.

ABSTRACT
Mitochondrial dysfunction and endoplasmic reticulum (ER) stress are closely associated with β-cell dysfunction and peripheral insulin resistance. Thus, each of these factors contributes to the development of type 2 diabetes mellitus (DM). The accumulated evidence reveals structural and functional communications between mitochondria and the ER. It is now well established that ER stress causes apoptotic cell death by disturbing mitochondrial Ca(2+) homeostasis. In addition, recent studies have shown that mitochondrial dysfunction causes ER stress. In this paper, we summarize the roles that mitochondrial dysfunction and ER stress play in the pathogenesis of type 2 DM. Structural and functional communications between mitochondria and the ER are also discussed. Finally, we focus on recent findings supporting the hypothesis that mitochondrial dysfunction and the subsequent induction of ER stress play important roles in the pathogenesis of type 2 DM.

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Roles of ER stress in the pathogenesis of β-cell apoptosis and insulin resistance.
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Related In: Results  -  Collection


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fig2: Roles of ER stress in the pathogenesis of β-cell apoptosis and insulin resistance.

Mentions: Several components of the UPR that contribute to β-cell apoptosis have been shown (Figure 2). ER stress can induce β-cell apoptosis through prolonged activation of IRE1-TRAF2-ASK1 cascade and JNK pathway [52]. CHOP also plays a crucial role in the induction of ER stress-mediated β-cell apoptosis [53].


Interaction between mitochondria and the endoplasmic reticulum: implications for the pathogenesis of type 2 diabetes mellitus.

Leem J, Koh EH - Exp Diabetes Res (2011)

Roles of ER stress in the pathogenesis of β-cell apoptosis and insulin resistance.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3140192&req=5

fig2: Roles of ER stress in the pathogenesis of β-cell apoptosis and insulin resistance.
Mentions: Several components of the UPR that contribute to β-cell apoptosis have been shown (Figure 2). ER stress can induce β-cell apoptosis through prolonged activation of IRE1-TRAF2-ASK1 cascade and JNK pathway [52]. CHOP also plays a crucial role in the induction of ER stress-mediated β-cell apoptosis [53].

Bottom Line: It is now well established that ER stress causes apoptotic cell death by disturbing mitochondrial Ca(2+) homeostasis.In addition, recent studies have shown that mitochondrial dysfunction causes ER stress.Structural and functional communications between mitochondria and the ER are also discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, University of Ulsan College of Medicine, 388-1 Poongnap-Dong, Songpa-Gu, Seoul 138-736, Republic of Korea.

ABSTRACT
Mitochondrial dysfunction and endoplasmic reticulum (ER) stress are closely associated with β-cell dysfunction and peripheral insulin resistance. Thus, each of these factors contributes to the development of type 2 diabetes mellitus (DM). The accumulated evidence reveals structural and functional communications between mitochondria and the ER. It is now well established that ER stress causes apoptotic cell death by disturbing mitochondrial Ca(2+) homeostasis. In addition, recent studies have shown that mitochondrial dysfunction causes ER stress. In this paper, we summarize the roles that mitochondrial dysfunction and ER stress play in the pathogenesis of type 2 DM. Structural and functional communications between mitochondria and the ER are also discussed. Finally, we focus on recent findings supporting the hypothesis that mitochondrial dysfunction and the subsequent induction of ER stress play important roles in the pathogenesis of type 2 DM.

Show MeSH
Related in: MedlinePlus