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Pancreatic beta cell targets represent a diverse group of proteins and receptors specifically or preferentially expressed on the surface or within the insulin-producing beta cells of the pancreatic islets (NIH, 2010) [1.1.1, 1.1.3]. These targets are critical for the regulation of glucose homeostasis through the synthesis and secretion of insulin (NIH, 2008) [1.1.4]. In drug discovery, they are categorized into those that stimulate insulin secretion, such as the glucagon-like peptide 1 receptor (GLP-1R) and ATP-sensitive potassium (KATP) channels, and those that promote beta cell proliferation and regeneration, such as DYRK1A (NIH, 2022) [1.2.1, 1.2.2]. Additionally, markers like zinc transporter 8 (ZnT8) and vesicular monoamine transporter 2 (VMAT2) serve as essential targets for non-invasive imaging of beta cell mass (Diabetes Journals, 2022; NIH, 2010) [1.1.2, 1.3.3]. Dysregulation or autoimmune destruction of these targets is central to the pathogenesis of Type 1 and Type 2 diabetes (NIH, 2014) [1.3.2]. Therapeutic strategies focusing on these targets aim to restore insulin production, protect beta cell function, or replenish lost beta cell mass through regenerative medicine (Frontiers, 2020) [1.2.3, 1.2.5].
Stimulation of insulin secretion via KATP channel closure or GLP-1 receptor activation, induction of beta cell proliferation through DYRK1A inhibition, and protection against beta cell apoptosis.
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