ArticleEndocrinology2017
Protective Role of Complement C3 Against Cytokine-Mediated β-Cell Apoptosis.
Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Beta-cell-specific C3 deficiency exacerbates metabolic dysregulation and insulin resistance in obesity.Molecular metabolism · 2026Article
- The secret life of complement: challenges and opportunities in exploring functions of the complosome in disease.The Journal of clinical investigation · 2025Review
- Complement activation at the interface between adipocytes and cancer cells drives tumor progression.JCI insight · 2025Article
- Bcl-2 and Bcl-xL in Diabetes: Contributions to Endocrine Pancreas Viability and Function.Biomedicines · 2025Review
- The complement system in human pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- Hypoxia-induced complement component 3 promotes aggressive tumor growth in the glioblastoma microenvironment.JCI insight · 2024Article
- Intracellular C3 protects β-cells from IL-1β-driven cytotoxicity via interaction with Fyn-related kinase.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Decrease in multiple complement proteins associated with development of islet autoimmunity and type 1 diabetes.iScience · 2024Article
- C3 deficiency promotes pulmonary inflammation in AT1R-induced mouse model for systemic sclerosis.Frontiers in immunology · 2024Article
- Systematic review of type 1 diabetes biomarkers reveals regulation in circulating proteins related to complement, lipid metabolism, and immune response.Clinical proteomics · 2023Review
- Article
- Inhibition of the type 1 diabetes candidate gene PTPN2 aggravates TNF-α-induced human beta cell dysfunction and death.Diabetologia · 2023Article
- BCL-XL Overexpression Protects Pancreatic β-Cells against Cytokine- and Palmitate-Induced Apoptosis.International journal of molecular sciences · 2023Article
- An in vitro approach to understand contribution of kidney cells to human urinary extracellular vesicles.Journal of extracellular vesicles · 2023Article
- The Complement System, Aging, and Aging-Related Diseases.International journal of molecular sciences · 2022Review
- Alternative translation and retrotranslocation of cytosolic C3 that detects cytoinvasive bacteria.Cellular and molecular life sciences : CMLS · 2022Article
- In Vitro Assays to Identify Metabolism-Disrupting Chemicals with Diabetogenic Activity in a Human Pancreatic β-Cell Model.International journal of molecular sciences · 2022Article
- High CD34 surface expression in BCP-ALL predicts poor induction therapy response and is associated with altered expression of genes related to cell migration and adhesion.Molecular oncology · 2022Article
- Accumulation of microbial DNAs promotes to islet inflammation and β cell abnormalities in obesity in mice.Nature communications · 2022Article
- As in Real Estate, Location Matters: Cellular Expression of Complement Varies Between Macular and Peripheral Regions of the Retina and Supporting Tissues.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Type 1 diabetes is a chronic autoimmune disease characterized by pancreatic islet inflammation and β-cell destruction by proinflammatory cytokines and other mediators. Based on RNA sequencing and protein-protein interaction analyses of human islets exposed to proinflammatory cytokines, we identified complement C3 as a hub for some of the effects of cytokines. The proinflammatory cytokines interleukin-1β plus interferon-γ increase C3 expression in rodent and human pancreatic β-cells, and C3 is detected by histology in and around the islets of diabetic patients. Surprisingly, C3 silencing exacerbates apoptosis under both basal condition and following exposure to cytokines, and it increases chemokine expression upon cytokine treatment. C3 exerts its prosurvival effects via AKT activation and c-Jun N-terminal kinase inhibition. Exogenously added C3 also protects against cytokine-induced β-cell death and partially rescues the deleterious effects of inhibition of endogenous C3. These data suggest that locally produced C3 is an important prosurvival mechanism in pancreatic β-cells under a proinflammatory assault.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.