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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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Related in: MedlinePlus

Bidirectional communication between dysfunctional mitochondria and the ER under stress contributes to the development of type 2 DM.
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fig3: Bidirectional communication between dysfunctional mitochondria and the ER under stress contributes to the development of type 2 DM.

Mentions: We have provided a brief overview of the interaction between mitochondrial dysfunction and ER stress. In particular, we examined the role played by such interaction in the pathogenesis of type 2 DM. Mitochondrial dysfunction and ER stress are essential for β-cell dysfunction and peripheral insulin resistance. To date, substantial progress has been made in understanding structural and functional communications between mitochondria and the ER. We now know that ER stress can induce mitochondrial dysfunction. Thus, such stress plays a central role in apoptosis signaling via Ca2+- and/or ROS-dependent mechanisms. Together with recent findings linking mitochondrial dysfunction and ER stress, it appears that bidirectional communication exists between these two organelles (Figure 3). Characterization of interactions between mitochondria and the ER is a dynamic and growing area of interest; future research will carefully dissect such processes. Hopefully, the studies will help us to gain a better understanding of the pathogenesis underlying type 2 DM. Therapeutic approach aimed at restoring mitochondria function will prevent or treat insulin resistance and type 2 DM through suppression of ER stress.


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

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

Bidirectional communication between dysfunctional mitochondria and the ER under stress contributes to the development of type 2 DM.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Bidirectional communication between dysfunctional mitochondria and the ER under stress contributes to the development of type 2 DM.
Mentions: We have provided a brief overview of the interaction between mitochondrial dysfunction and ER stress. In particular, we examined the role played by such interaction in the pathogenesis of type 2 DM. Mitochondrial dysfunction and ER stress are essential for β-cell dysfunction and peripheral insulin resistance. To date, substantial progress has been made in understanding structural and functional communications between mitochondria and the ER. We now know that ER stress can induce mitochondrial dysfunction. Thus, such stress plays a central role in apoptosis signaling via Ca2+- and/or ROS-dependent mechanisms. Together with recent findings linking mitochondrial dysfunction and ER stress, it appears that bidirectional communication exists between these two organelles (Figure 3). Characterization of interactions between mitochondria and the ER is a dynamic and growing area of interest; future research will carefully dissect such processes. Hopefully, the studies will help us to gain a better understanding of the pathogenesis underlying type 2 DM. Therapeutic approach aimed at restoring mitochondria function will prevent or treat insulin resistance and type 2 DM through suppression of ER stress.

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