Islet amyloid toxicity: From genesis to counteracting mechanisms
| Autor: | Carine Marmentini, Antonio C. Boschero, Mirian Ayumi Kurauti, Renato Chaves Souto Branco |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Amyloid
endocrine system Programmed cell death endocrine system diseases Physiology Clinical Biochemistry Amylin Inflammation Islets of Langerhans Insulin-Secreting Cells mental disorders medicine Extracellular Animals Humans Insulin geography geography.geographical_feature_category Chemistry Endoplasmic reticulum Autophagy Cell Biology Islet Islet Amyloid Polypeptide Diabetes Mellitus Type 2 Cancer research medicine.symptom |
| Zdroj: | Journal of Cellular Physiology. 237:1119-1142 |
| ISSN: | 1097-4652 0021-9541 |
| DOI: | 10.1002/jcp.30600 |
| Popis: | Islet amyloid polypeptide (IAPP or amylin) is a hormone co-secreted with insulin by pancreatic β-cells and is the major component of islet amyloid. Islet amyloid is found in the pancreas of patients with type 2 diabetes (T2D) and may be involved in β-cell dysfunction and death, observed in this disease. Thus, investigating the aspects related to amyloid formation is relevant to the development of strategies towards β-cell protection. In this sense, IAPP misprocessing, IAPP overproduction, and disturbances in intra- and extracellular environments seem to be decisive for IAPP to form islet amyloid. Islet amyloid toxicity in β-cells may be triggered in intra- and/or extracellular sites by membrane damage, endoplasmic reticulum stress, autophagy disruption, mitochondrial dysfunction, inflammation, and apoptosis. Importantly, different approaches have been suggested to prevent islet amyloid cytotoxicity, from inhibition of IAPP aggregation to attenuation of cell death mechanisms. Such approaches have improved β-cell function and prevented the development of hyperglycemia in animals. Therefore, counteracting islet amyloid may be a promising therapy for T2D treatment. |
| Databáze: | OpenAIRE |
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