The role of vitamin D signalling in β cell apoptosis: a systematic review
Li D, Norris N, An Y, Gunton JE
Apoptosis : an international journal on programmed cell death · 0 citas
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- Revisión sistemática (indexado por PubMed)
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Quién lo pagó
- Financiación
- Financiación independiente
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Publicación
- Publicado
- 2026-10-01 · Apoptosis · vol. 31 · número 10
- Editorial
- Springer Science+Business Media
- Citado
- 0 citas · más que el 75% de estudios similares · 0.0× el promedio de su campo
- Referencias
- 120 trabajos
- Acceso
- Acceso abierto (revista híbrida) · CC-BY
- Áreas de investigación
- Pancreatic function and diabetes · Vitamin D Research Studies · Cell death mechanisms and regulation
- Palabras clave
- vitamin D receptor, pancreatic beta-cell apoptosis, beta-cell survival, vitamin D analogs, 1,25-dihydroxyvitamin D3, NF-κB signaling, oxidative stress, glucotoxicity, lipotoxicity, streptozotocin, endoplasmic reticulum stress, pyroptosis, ferroptosis, autophagy, Bcl-2 family proteins, mitochondrial stability, insulin secretion, beta-cell mass, diabetes mellitus
- MeSH
- animals, humans, vitamin d, receptors, calcitriol, signal transduction, apoptosis, oxidative stress, insulin-secreting cells
4 autores
- Donglai Li🇦🇺The University of Sydney; Westmead Institute for Medical Research
- Nicholas Norris🇦🇺The University of Sydney; Westmead Institute for Medical Research
- Yousun An🇦🇺The University of Sydney; Westmead Institute for Medical Research
- Jenny Elizabeth Gunton🇦🇺 · autor de correspondenciaThe University of Sydney; Westmead Hospital; Westmead Institute for Medical Research
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Vitamin D signalling, primarily through the vitamin D receptor (VDR), regulates cellular survival and programmed cell death. This systematic review aims to synthesise current evidence on the role of vitamin D in pancreatic β-cell apoptosis.
Methods
Medline, Embase, and Scopus were searched for original studies investigating vitamin D, vitamin D analogues, or VDR-related interventions in experimental models of β-cell apoptosis or programmed cell death.
Results
26 studies were included. Across in vitro, ex vivo, and in vivo models, vitamin D signalling protected β-cells against apoptosis induced by cytokine-mediated inflammation, oxidative stress, glucotoxicity, lipotoxicity, streptozotocin exposure, and diabetic stress. These effects were associated with reduced NF-κB signalling, nitric oxide and reactive oxygen species production, improved mitochondrial stability, modulation of Bcl-2 family proteins, inhibition of endoplasmic reticulum stress, and regulation of pyroptosis, ferroptosis, and autophagy-related survival mechanisms. VDR activation also supported β-cell identity, insulin secretion, and β-cell mass preservation. In contrast, calcitriol-associated growth inhibition and increased apoptosis were reported in βTC insulinoma models.
Conclusion
Vitamin D signalling generally appears cytoprotective in β-cells exposed to inflammatory, oxidative, and metabolic stress. However, its effects on β-cell survival are model- and context-dependent, reflecting differences in cellular background, experimental stressors, and methods used to assess cell death.
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