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Updated: Aug 26, 2025

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
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Are off-target effects of imatinib the key to improving beta-cell function in diabetes?

Nils Welsh1

  • 1Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.

Upsala Journal of Medical Sciences
|October 3, 2022
PubMed

The small tyrosine kinase (TK) inhibitor imatinib mesylate (Gleevec, STI571) protects against both type 1 and type 2 diabetes, but as it inhibits many TKs and other proteins, it is not clear by which mechanisms it acts. This present review will focus on the possibility that imatinib acts, at least in part, by improving beta-cell function and survival via off-target effects on beta-cell signaling/metabolic flow events. Particular attention will be given to the possibility that imatinib and other TK inhibitors function as inhibitors of mitochondrial respiration. A better understanding of how imatinib counteracts diabetes will possibly help to clarify the pathogenic role of beta-cell signaling events and mitochondrial function, and hopefully leading to improved treatment of the disease.

Keywords:
Pancreatic beta-cellsimatinibmitochondriatype 1 diabetestype 2 diabetestyrosine kinase inhibitor

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