Ryanodine Receptors in Islet Cell Function: Calcium Signaling, Hormone Secretion, and Diabetes
Ryanodine receptors (RyRs) are large intracellular Ca2+ release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic islet endocrine cells. This review examines the role of RyRs in islet cell function, focusing on calcium signaling and hormone secretion, wh...
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| Vydáno v: | Cells (Basel, Switzerland) Ročník 14; číslo 10; s. 690 |
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MDPI AG
10.05.2025
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| ISSN: | 2073-4409, 2073-4409 |
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| Abstract | Ryanodine receptors (RyRs) are large intracellular Ca2+ release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic islet endocrine cells. This review examines the role of RyRs in islet cell function, focusing on calcium signaling and hormone secretion, while addressing the ongoing debate regarding their significance due to their limited expression. We explore conflicting experimental results and their potential causes, synthesizing current knowledge on RyR isoforms in islet cells, particularly in beta and delta cells. The review discusses how RyR-mediated calcium-induced calcium release enhances, rather than drives, glucose-stimulated insulin secretion. We examine the phosphorylation-dependent regulation of beta-cell RyRs, the concept of “leaky ryanodine receptors”, and the roles of RyRs in endoplasmic reticulum stress, apoptosis, store-operated calcium entry, and beta-cell electrical activity. The relationship between RyR dysfunction and the development of impaired insulin secretion in diabetes is assessed, noting their limited role in human diabetes pathogenesis given the disease’s polygenic nature. We highlight the established role of RyR-mediated CICR in the mechanism of action of common type 2 diabetes treatments, such as glucagon-like peptide-1, which enhances insulin secretion. By integrating findings from electrophysiological, molecular, and clinical studies, this review provides a balanced perspective on RyRs in islet cell physiology and pathology, emphasizing their significance in both normal insulin secretion and current diabetes therapies. |
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| AbstractList | Ryanodine receptors (RyRs) are large intracellular Ca[sup.2+] release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic islet endocrine cells. This review examines the role of RyRs in islet cell function, focusing on calcium signaling and hormone secretion, while addressing the ongoing debate regarding their significance due to their limited expression. We explore conflicting experimental results and their potential causes, synthesizing current knowledge on RyR isoforms in islet cells, particularly in beta and delta cells. The review discusses how RyR-mediated calcium-induced calcium release enhances, rather than drives, glucose-stimulated insulin secretion. We examine the phosphorylation-dependent regulation of beta-cell RyRs, the concept of “leaky ryanodine receptors”, and the roles of RyRs in endoplasmic reticulum stress, apoptosis, store-operated calcium entry, and beta-cell electrical activity. The relationship between RyR dysfunction and the development of impaired insulin secretion in diabetes is assessed, noting their limited role in human diabetes pathogenesis given the disease’s polygenic nature. We highlight the established role of RyR-mediated CICR in the mechanism of action of common type 2 diabetes treatments, such as glucagon-like peptide-1, which enhances insulin secretion. By integrating findings from electrophysiological, molecular, and clinical studies, this review provides a balanced perspective on RyRs in islet cell physiology and pathology, emphasizing their significance in both normal insulin secretion and current diabetes therapies. Ryanodine receptors (RyRs) are large intracellular Ca2+ release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic islet endocrine cells. This review examines the role of RyRs in islet cell function, focusing on calcium signaling and hormone secretion, while addressing the ongoing debate regarding their significance due to their limited expression. We explore conflicting experimental results and their potential causes, synthesizing current knowledge on RyR isoforms in islet cells, particularly in beta and delta cells. The review discusses how RyR-mediated calcium-induced calcium release enhances, rather than drives, glucose-stimulated insulin secretion. We examine the phosphorylation-dependent regulation of beta-cell RyRs, the concept of “leaky ryanodine receptors”, and the roles of RyRs in endoplasmic reticulum stress, apoptosis, store-operated calcium entry, and beta-cell electrical activity. The relationship between RyR dysfunction and the development of impaired insulin secretion in diabetes is assessed, noting their limited role in human diabetes pathogenesis given the disease’s polygenic nature. We highlight the established role of RyR-mediated CICR in the mechanism of action of common type 2 diabetes treatments, such as glucagon-like peptide-1, which enhances insulin secretion. By integrating findings from electrophysiological, molecular, and clinical studies, this review provides a balanced perspective on RyRs in islet cell physiology and pathology, emphasizing their significance in both normal insulin secretion and current diabetes therapies. Ryanodine receptors (RyRs) are large intracellular Ca2+ release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic islet endocrine cells. This review examines the role of RyRs in islet cell function, focusing on calcium signaling and hormone secretion, while addressing the ongoing debate regarding their significance due to their limited expression. We explore conflicting experimental results and their potential causes, synthesizing current knowledge on RyR isoforms in islet cells, particularly in beta and delta cells. The review discusses how RyR-mediated calcium-induced calcium release enhances, rather than drives, glucose-stimulated insulin secretion. We examine the phosphorylation-dependent regulation of beta-cell RyRs, the concept of "leaky ryanodine receptors", and the roles of RyRs in endoplasmic reticulum stress, apoptosis, store-operated calcium entry, and beta-cell electrical activity. The relationship between RyR dysfunction and the development of impaired insulin secretion in diabetes is assessed, noting their limited role in human diabetes pathogenesis given the disease's polygenic nature. We highlight the established role of RyR-mediated CICR in the mechanism of action of common type 2 diabetes treatments, such as glucagon-like peptide-1, which enhances insulin secretion. By integrating findings from electrophysiological, molecular, and clinical studies, this review provides a balanced perspective on RyRs in islet cell physiology and pathology, emphasizing their significance in both normal insulin secretion and current diabetes therapies.Ryanodine receptors (RyRs) are large intracellular Ca2+ release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic islet endocrine cells. This review examines the role of RyRs in islet cell function, focusing on calcium signaling and hormone secretion, while addressing the ongoing debate regarding their significance due to their limited expression. We explore conflicting experimental results and their potential causes, synthesizing current knowledge on RyR isoforms in islet cells, particularly in beta and delta cells. The review discusses how RyR-mediated calcium-induced calcium release enhances, rather than drives, glucose-stimulated insulin secretion. We examine the phosphorylation-dependent regulation of beta-cell RyRs, the concept of "leaky ryanodine receptors", and the roles of RyRs in endoplasmic reticulum stress, apoptosis, store-operated calcium entry, and beta-cell electrical activity. The relationship between RyR dysfunction and the development of impaired insulin secretion in diabetes is assessed, noting their limited role in human diabetes pathogenesis given the disease's polygenic nature. We highlight the established role of RyR-mediated CICR in the mechanism of action of common type 2 diabetes treatments, such as glucagon-like peptide-1, which enhances insulin secretion. By integrating findings from electrophysiological, molecular, and clinical studies, this review provides a balanced perspective on RyRs in islet cell physiology and pathology, emphasizing their significance in both normal insulin secretion and current diabetes therapies. Ryanodine receptors (RyRs) are large intracellular Ca 2+ release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic islet endocrine cells. This review examines the role of RyRs in islet cell function, focusing on calcium signaling and hormone secretion, while addressing the ongoing debate regarding their significance due to their limited expression. We explore conflicting experimental results and their potential causes, synthesizing current knowledge on RyR isoforms in islet cells, particularly in beta and delta cells. The review discusses how RyR-mediated calcium-induced calcium release enhances, rather than drives, glucose-stimulated insulin secretion. We examine the phosphorylation-dependent regulation of beta-cell RyRs, the concept of "leaky ryanodine receptors", and the roles of RyRs in endoplasmic reticulum stress, apoptosis, store-operated calcium entry, and beta-cell electrical activity. The relationship between RyR dysfunction and the development of impaired insulin secretion in diabetes is assessed, noting their limited role in human diabetes pathogenesis given the disease's polygenic nature. We highlight the established role of RyR-mediated CICR in the mechanism of action of common type 2 diabetes treatments, such as glucagon-like peptide-1, which enhances insulin secretion. By integrating findings from electrophysiological, molecular, and clinical studies, this review provides a balanced perspective on RyRs in islet cell physiology and pathology, emphasizing their significance in both normal insulin secretion and current diabetes therapies. Ryanodine receptors (RyRs) are large intracellular Ca release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic islet endocrine cells. This review examines the role of RyRs in islet cell function, focusing on calcium signaling and hormone secretion, while addressing the ongoing debate regarding their significance due to their limited expression. We explore conflicting experimental results and their potential causes, synthesizing current knowledge on RyR isoforms in islet cells, particularly in beta and delta cells. The review discusses how RyR-mediated calcium-induced calcium release enhances, rather than drives, glucose-stimulated insulin secretion. We examine the phosphorylation-dependent regulation of beta-cell RyRs, the concept of "leaky ryanodine receptors", and the roles of RyRs in endoplasmic reticulum stress, apoptosis, store-operated calcium entry, and beta-cell electrical activity. The relationship between RyR dysfunction and the development of impaired insulin secretion in diabetes is assessed, noting their limited role in human diabetes pathogenesis given the disease's polygenic nature. We highlight the established role of RyR-mediated CICR in the mechanism of action of common type 2 diabetes treatments, such as glucagon-like peptide-1, which enhances insulin secretion. By integrating findings from electrophysiological, molecular, and clinical studies, this review provides a balanced perspective on RyRs in islet cell physiology and pathology, emphasizing their significance in both normal insulin secretion and current diabetes therapies. |
| Audience | Academic |
| Author | Islam, Md. Shahidul |
| AuthorAffiliation | 2 Department of Internal Medicine, Uppsala University Hospital, SE-751 85 Uppsala, Sweden 1 Karolinska Institutet, Department of Clinical Sciences and Education, Södersjukhuset, Research Center, 5th Floor, SE-118 83 Stockholm, Sweden; shahidul.islam@ki.se ; Tel.: +46-70-259-3446 |
| AuthorAffiliation_xml | – name: 1 Karolinska Institutet, Department of Clinical Sciences and Education, Södersjukhuset, Research Center, 5th Floor, SE-118 83 Stockholm, Sweden; shahidul.islam@ki.se ; Tel.: +46-70-259-3446 – name: 2 Department of Internal Medicine, Uppsala University Hospital, SE-751 85 Uppsala, Sweden |
| Author_xml | – sequence: 1 givenname: Md. Shahidul orcidid: 0000-0002-9016-1881 surname: Islam fullname: Islam, Md. Shahidul |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40422193$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-560582$$DView record from Swedish Publication Index (Uppsala universitet) |
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| Keywords | ryanodine receptors in delta cells ryanodine receptors and diabetes endoplasmic reticulum stress in beta cells ryanodine receptors and store-operated calcium entry beta-cell electrical activity and ryanodine receptors calcium signaling in beta cells calcium-induced calcium release in islet cells glucagon-like peptide-1 and ryanodine receptors ryanodine receptors in islets cells ryanodine receptors and insulin secretion |
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| Snippet | Ryanodine receptors (RyRs) are large intracellular Ca2+ release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic... Ryanodine receptors (RyRs) are large intracellular Ca release channels primarily found in muscle and nerve cells and also present at low levels in pancreatic... Ryanodine receptors (RyRs) are large intracellular Ca[sup.2+] release channels primarily found in muscle and nerve cells and also present at low levels in... Ryanodine receptors (RyRs) are large intracellular Ca 2+ release channels primarily found in muscle and nerve cells and also present at low levels in... |
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| SubjectTerms | Agonists Animals Apoptosis Beta cells beta-cell electrical activity and ryanodine receptors Caffeine Calcium (intracellular) Calcium (reticular) Calcium - metabolism Calcium channels Calcium release channels Calcium Signaling calcium signaling in beta cells Calcium signalling calcium-induced calcium release in islet cells Delta cells Dextrose Diabetes mellitus (non-insulin dependent) Diabetes Mellitus - metabolism Diabetes Mellitus, Type 2 - metabolism Endoplasmic reticulum endoplasmic reticulum stress in beta cells Enzymes Experiments Glucagon Glucagon-like peptide 1 glucagon-like peptide-1 and ryanodine receptors Glucose Hormones - metabolism Humans Insulin Insulin Secretion Insulin-Secreting Cells - metabolism Intracellular signalling Islet cells Islets of Langerhans - metabolism Isoforms Neurons Pathogenesis Phosphorylation Receptor mechanisms Review Ryanodine Receptor Calcium Release Channel - metabolism Ryanodine receptors ryanodine receptors and diabetes ryanodine receptors and insulin secretion ryanodine receptors and store-operated calcium entry ryanodine receptors in delta cells ryanodine receptors in islets cells Type 2 diabetes |
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| Title | Ryanodine Receptors in Islet Cell Function: Calcium Signaling, Hormone Secretion, and Diabetes |
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