{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T08:21:41Z","timestamp":1787559701700,"version":"build-2736575974"},"reference-count":224,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T00:00:00Z","timestamp":1787529600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa Do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2024\/17148-5"],"award-info":[{"award-number":["2024\/17148-5"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Netw. Physiol."],"abstract":"<jats:p>\n                    Two of the main intracellular signaling molecules in pancreatic \u03b2-cells are calcium (Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ) and reactive oxygen species (ROS). Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signaling is essential for regulating energy metabolism, insulin secretion, and the modulation of key factors involved in \u03b2-cell survival and function. In parallel, redox signaling also affects energy metabolism and enhances glucose-stimulated insulin secretion. Imbalances in Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and redox signaling may contribute to the development of various pathological conditions, including type 2 diabetes mellitus (T2D). T2D is one of the most prevalent diseases worldwide and is characterized by a progressive decline in insulin secretion, typically in the context of obesity and insulin resistance in target tissues. Insulin resistance and poor glycemic control lead to the development of several complications, such as retinopathy, kidney dysfunction, and neuropathy, which negatively impact both quality and life expectancy. Understanding how Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and ROS are modulated during the progression of T2D may aid in the development of pharmacological strategies aimed at preventing \u03b2-cell dysfunction or promoting their functional recovery. The two main intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    stores in \u03b2-cells are the endoplasmic reticulum (ER) and mitochondria, while two important sources of ROS are mitochondria and NADPH oxidase (NOX) enzymes. It is also known that ROS and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    interact bidirectionally: Ca\n                    <jats:sup>2+<\/jats:sup>\n                    can stimulate oxidative phosphorylation, increasing mitochondrial ROS production; some mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channels are redox-sensitive; certain Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -dependent enzymes respond to redox signals; and some NOX isoforms are activated by Ca\n                    <jats:sup>2+<\/jats:sup>\n                    . Thus, ROS can modulate Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signaling, while Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signaling is essential for ROS production, establishing a feedback loop that affects \u03b2-cell function and survival. The aim of this review is to summarize the main findings on Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and ROS in pancreatic \u03b2-cells, addressing each of these signaling systems separately in physiological conditions and in T2D, and subsequently discussing their functional interaction and how these mechanisms function within the islet network. We also highlight the integration of the different intracellular compartments involved in these processes, namely, the ER, mitochondria, and NOX enzymes.\n                  <\/jats:p>","DOI":"10.3389\/fnetp.2026.1864821","type":"journal-article","created":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T07:59:26Z","timestamp":1787558366000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Organelle-specific crosstalk between calcium and redox signaling in pancreatic \u03b2-cells in physiology and type 2 diabetes"],"prefix":"10.3389","volume":"6","author":[{"given":"Lucas Rafael Pereira","family":"Camara","sequence":"first","affiliation":[{"name":"Department of Clinical and Toxicological Analysis, School of Pharmaceutical Sciences, University of Sao Paulo","place":["Sao Paulo, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eloisa Aparecida","family":"Vilas-Boas","sequence":"additional","affiliation":[{"name":"Department of Clinical and Toxicological Analysis, School of Pharmaceutical Sciences, University of Sao Paulo","place":["Sao Paulo, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,24]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"147","DOI":"10.1007\/s00592-008-0033-z","article-title":"Adipocytes in subjects with impaired fasting glucose and impaired glucose tolerance are resistant to the anti-lipolytic effect of insulin","volume":"45","author":"Abdul-Ghani","year":"2008","journal-title":"Acta Diabetol."},{"key":"B2","doi-asserted-by":"publisher","first-page":"282","DOI":"10.1007\/s00125-004-1627-9","article-title":"Functional and morphological alterations of mitochondria in pancreatic beta cells from type 2 diabetic patients","volume":"48","author":"Anello","year":"2005","journal-title":"Diabetologia"},{"key":"B3","doi-asserted-by":"publisher","first-page":"1308","DOI":"10.3109\/10715762.2015.1067697","article-title":"The novel NADPH oxidase 4 inhibitor GLX351322 counteracts glucose intolerance in high-fat diet-treated C57BL\/6 mice","volume":"49","author":"Anvari","year":"2015","journal-title":"Free Radic. 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