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mTORC1 Signaling: A Double-Edged Sword in Diabetic β Cells (2017)
Journal Article
Ardestani, A., Lupse, B., Kido, Y., Leibowitz, G., & Maedler, K. (2018). mTORC1 Signaling: A Double-Edged Sword in Diabetic β Cells. Cell Metabolism, 27(2), 314-331. https://doi.org/10.1016/j.cmet.2017.11.004

The mechanistic target of rapamycin complex 1 (mTORC1) is a central regulator of metabolic and nutrient cues that integrates environmental inputs into downstream signaling pathways to control cellular metabolism, growth, and survival. While numerous... Read More about mTORC1 Signaling: A Double-Edged Sword in Diabetic β Cells.

The Hippo signaling pathway in pancreatic β-cells: Functions and regulations (2017)
Journal Article
Ardestani, A., & Maedler, K. (2018). The Hippo signaling pathway in pancreatic β-cells: Functions and regulations. Endocrine Reviews, 39(1), 21-35. https://doi.org/10.1210/er.2017-00167

Hippo signaling is an evolutionarily conserved pathway that critically regulates development and homeostasis of various tissues in response to a wide range of extracellular and intracellular signals. As an emerging important player in many diseases,... Read More about The Hippo signaling pathway in pancreatic β-cells: Functions and regulations.

mTORC in β cells: More Than Only Recognizing Comestibles (2017)
Journal Article
Maedler, K., & Ardestani, A. (2017). mTORC in β cells: More Than Only Recognizing Comestibles. Journal of Cell Biology, 216(7), 1883-1885. https://doi.org/10.1083/jcb.201704179

The pathways regulating pancreatic β cell survival in diabetes are poorly understood. Here, Chau et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201701085) demonstrate that mTOR regulates the apoptotic machinery through binding to the ChREBP-... Read More about mTORC in β cells: More Than Only Recognizing Comestibles.

Reciprocal regulation of mTOR complexes in pancreatic islets from humans with type 2 diabetes (2016)
Journal Article
Yuan, T., Rafizadeh, S., Gorrepati, K. D. D., Lupse, B., Oberholzer, J., Maedler, K., & Ardestani, A. (2017). Reciprocal regulation of mTOR complexes in pancreatic islets from humans with type 2 diabetes. Diabetologia, 60(4), 668-678. https://doi.org/10.1007/s00125-016-4188-9

Aims/hypothesis: Mechanistic target of rapamycin complex 1 (mTORC1) is a master regulator of nutritional status at the cellular and organismic level. While mTORC1 mediates beta cell growth and expansion, its hyperactivation has been observed in pancr... Read More about Reciprocal regulation of mTOR complexes in pancreatic islets from humans with type 2 diabetes.

Proproliferative and antiapoptotic action of exogenously introduced YAP in pancreatic β cells (2016)
Journal Article
Yuan, T., Rafizadeh, S., Azizi, Z., Lupse, B., Devi Gorrepati, K. D., Awal, S., …Ardestani, A. (2016). Proproliferative and antiapoptotic action of exogenously introduced YAP in pancreatic β cells. JCI Insight, 1(18), Article e86326. https://doi.org/10.1172/jci.insight.86326

Loss of functional pancreatic β cells is a hallmark of both type 1 and 2 diabetes. Identifying the pathways that promote β cell proliferation and/or block β cell apoptosis is a potential strategy for diabetes therapy. The transcriptional coactivator... Read More about Proproliferative and antiapoptotic action of exogenously introduced YAP in pancreatic β cells.

Angiopoetin-2 signals do not mediate the hypervascularization of islets in type 2 diabetes (2016)
Journal Article
Shah, P., Lueschen, N., Ardestani, A., Oberholzer, J., Olerud, J., Carlsson, P. O., & Maedler, K. (2016). Angiopoetin-2 signals do not mediate the hypervascularization of islets in type 2 diabetes. PLoS ONE, 11(9), Article e0161834. https://doi.org/10.1371/journal.pone.0161834

Aims Changes in the islet vasculature have been implicated in the regulation of β-cell survival and function during the progression to type 2 diabetes (T2D). Failure of the β-cell to compensate for the increased insulin demand in obesity eventually l... Read More about Angiopoetin-2 signals do not mediate the hypervascularization of islets in type 2 diabetes.

β-MSCs: Successful fusion of MSCs with β-cells results in a β-cell like phenotype (2016)
Journal Article
Azizi, Z., Lange, C., Paroni, F., Ardestani, A., Meyer, A., Wu, Y., …Maedler, K. (2016). β-MSCs: Successful fusion of MSCs with β-cells results in a β-cell like phenotype. Oncotarget, 7(31), 48963-48977. https://doi.org/10.18632/oncotarget.10214

Bone marrow mesenchymal stromal cells (MSC) have anti-inflammatory, antiapoptotic and immunosuppressive properties and are a potent source for cell therapy. Cell fusion has been proposed for rapid generation of functional new reprogrammed cells. In t... Read More about β-MSCs: Successful fusion of MSCs with β-cells results in a β-cell like phenotype.

MST1: a promising therapeutic target to restore functional beta cell mass in diabetes (2016)
Journal Article
Ardestani, A., & Maedler, K. (2016). MST1: a promising therapeutic target to restore functional beta cell mass in diabetes. Diabetologia, 59(9), 1843-1849. https://doi.org/10.1007/s00125-016-3892-9

The loss of insulin-producing beta cells by apoptosis is a hallmark of all forms of diabetes mellitus. Strategies to prevent beta cell apoptosis and dysfunction are urgently needed to restore the insulin-producing cells and to prevent severe diabetes... Read More about MST1: a promising therapeutic target to restore functional beta cell mass in diabetes.

MST1 is a key regulator of beta cell apoptosis and dysfunction in diabetes (2014)
Journal Article
Ardestani, A., Paroni, F., Azizi, Z., Kaur, S., Khobragade, V., Yuan, T., …Maedler, K. (2014). MST1 is a key regulator of beta cell apoptosis and dysfunction in diabetes. Nature Medicine, 20(4), 385-397. https://doi.org/10.1038/nm.3482

Apoptotic cell death is a hallmark of the loss of insulin-producing beta cells in all forms of diabetes mellitus. Current treatments fail to halt the decline in functional beta cell mass, and strategies to prevent beta cell apoptosis and dysfunction... Read More about MST1 is a key regulator of beta cell apoptosis and dysfunction in diabetes.

The DPP-4 inhibitor linagliptin restores β-cell function and survival in human isolated islets through GLP-1 stabilization (2013)
Journal Article
Shah, P., Ardestani, A., Dharmadhikari, G., Laue, S., Schumann, D. M., Kerr-Conte, J., …Maedler, K. (2013). The DPP-4 inhibitor linagliptin restores β-cell function and survival in human isolated islets through GLP-1 stabilization. Journal of Clinical Endocrinology and Metabolism, 98(7), E1163–E1172. https://doi.org/10.1210/jc.2013-1029

Context: Inhibition of dipeptidyl peptidase-4 (DPP-4) is a potent strategy to increase glucose-dependent insulinotropic polypeptide and glucagon like peptide 1 (GLP-1) induced insulin secretion in diabetes. It is important to know whether new drugs a... Read More about The DPP-4 inhibitor linagliptin restores β-cell function and survival in human isolated islets through GLP-1 stabilization.