Advanced search

Filter By:

Journal Check one or more journals to show results from those journals only.

Choose more journals

Article type Check one or more article types to show results from those article types only.
Subject Check one or more subjects to show results from those subjects only.
Date Choose a date option to show results from those dates only.

Custom date range

Clear all filters
Sort by:
Showing 1–12 of 12 results
Advanced filters: Author: Kathrin Maedler Clear advanced filters

  • Type 1 diabetes (T1D) and type 2 diabetes (T2D) are both hallmarked by loss of insulin-producing pancreatic beta cells. Kathrin Maedler and her colleagues now show that the kinase MST1 is upregulated by diabetic conditions in beta cells, resulting in their dysfunction and their apoptosis. They also show that genetic knockout of the gene encoding Mst1 results in protection from diabetes in T1D and T2D mouse models.

    • Amin Ardestani
    • Federico Paroni
    • Kathrin Maedler
    Research
    Nature Medicine
    Volume: 20, P: 385-397

  • Viruses such as coxsackievirus B (CVB) have been associated with type I diabetes (T1D) and islet destruction. Here the authors show that Yes-associated protein (YAP) is upregulated in the whole pancreas in T1D and at-risk autoantibody (AAb + ) organ donors and that YAP over-expression enhances CVB replication, islet inflammation and β-cell apoptosis and suggest exocrine-islet-immune interactions as targeted interventions for T1D.

    • Shirin Geravandi
    • Huan Liu
    • Amin Ardestani
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-26

  • Diabetes is characterized by dysfunction and loss of beta-cells, and promoting beta-cell survival is of therapeutic interest. Here the authors show that Large-tumor suppressor 2 (LATS2), a core component of the Hippo signaling pathway, induces beta-cell failure through mTORC1 hyperactivation and autophagic flux suppression.

    • Ting Yuan
    • Karthika Annamalai
    • Amin Ardestani
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-18

  • Type 1 as well as type 2 diabetes are characterized by a loss of insulin-producing β-cells. Here the authors show that the FDA-approved drug neratinib has beneficial effects on β-cell survival, insulin secretion, and glycemic control in mouse models of diabetes.

    • Amin Ardestani
    • Sijia Li
    • Kathrin Maedler
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-17

  • Obesity is associated with mitochondrial dysfunction and chronic metabolic derailment. Cho et al. report that elevated adipose expression of the Hippo kinases STK3 and STK4 (STK3/4) in obesity and type 2 diabetes decreases the mass and oxidative capacity of adipocyte mitochondria. Genetic or pharmacological inhibition of STK3/4 restores mitochondrial mass and function in adipocytes and improves glucose homeostasis in mice with diet-induced obesity. These findings support STK3/4 as new targets for obesity-related diseases.

    • Kathrin Maedler
    • Amin Ardestani
    News & Views
    Nature Metabolism
    Volume: 3, P: 295-296

  • The Pleckstrin homology domain leucine-rich repeat protein phosphatases (PHLPPs) are novel therapeutic targets for the restoration of β-cell survival and function in diabetes. Their upregulation and activation in β-cells under conditions of both type 1 and type 2 diabetes directly correlates with β-cell failure; β-cell death and loss of insulin secretory function through disturbance of cell survival control mechanisms. PHLPPs directly dephosphorylate and regulate activities of β-cell survival-dependent kinases AKT and MST1 constituting a regulatory triangle loop to control β-cell apoptosis. PHLPP1 deletion in severely diabetic leptin receptor-deficient db/db mice restored normoglycemia and β-cell area through increased β-cell proliferation and reduced β-cell apoptosis. The beneficial effects of PHLPP1 deficiency in a severe mouse model of obesity and diabetes make PHLPP a new target for β-cell-directed diabetes therapy.

    • Blaz Lupse
    • Nick Heise
    • Amin Ardestani
    Comments & OpinionOpen Access
    Cell Death Discovery
    Volume: 8, P: 1-4