ReviewMolecular biology reports2025
Role of inflammasomes in diabetes mellitus: mechanisms, complications, and therapeutic potential.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Inflammasome Suppression via Combined Training Modulates Downstream Cytokines (Interleukin-1β/Caspase-1) and Improves Insulin Resistance in Diabetic Rats.Iranian journal of medical sciences · 2026Article
- Revisiting Insulin Resistance in the Pathophysiology of Type 2 Diabetes Mellitus: A Multi-Organ Perspective.Diabetes & metabolism journal · 2026Review
- Role of NLRP3 Inflammasome Inhibitors in Endothelial Dysfunction and Vascular Repair.Antioxidants (Basel, Switzerland) · 2026Review
- From sugar to flames: the detrimental role of pyroptosis in diabetes-associated bone loss.Molecular biology reports · 2026Review
- CD4Frontiers in immunology · 2026Review
- Regulatory Roles of Noncanonical Inflammasomes in Diabetes Mellitus and Diabetes-Associated Complications.International journal of molecular sciences · 2025Review
- Free prostate-specific antigen, total prostate-specific antigen, and their ratio associated with diabetic kidney disease: new evidence from male patients with diabetes in the United States.European journal of medical research · 2025Article
- Inulin andFrontiers in endocrinology · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Diabetes mellitus (DM) is a chronic metabolic disease characterized by insulin resistance and hyperglycemia. Emerging evidence suggests that chronic inflammation is central to the development of diabetes and associated complications. Inflammasomes, multi-protein complexes, are key regulators of the innate immune response. The pro-inflammatory cytokines such as interleukin-1β (IL-1β) and interleukin-18 (IL-18) are released upon activation. This causes inflammation in DM. This review aims to explain the mechanisms leading to the activation of inflammasomes and the regulation of different inflammasome isoforms concerning DM and related complications such as cardiovascular disease, neuropathy, nephropathy, and retinopathy. We will also explore the impact of metabolic factors like hyperglycemia and insulin resistance on activating inflammasomes. A better understanding of the interplay between different inflammasome isoforms and DM can help develop novel therapeutic strategies that target inflammasome pathways for preventing and treating complications associated with diabetes.
Indexed as
Identifiers
40544214What 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.