ArticleEndocrinology2017
Aldose Reductase Mediates NLRP3 Inflammasome-Initiated Innate Immune Response in Hyperglycemia-Induced Thp1 Monocytes and Male Mice.
Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 61 citations in OpenAlex.
- Immunometabolic regulation of cardiac macrophages in heart failure with preserved ejection fraction.Frontiers in immunology · 2026Review
- Metabolic and Vascular Inflammation in Alopecia Areata: Linking Uric Acid, Lipid Imbalance and ICAM-1 Upregulation.Experimental dermatology · 2025Article
- The Role and the Regulation of NLRP3 Inflammasome in Irritable Bowel Syndrome: A Narrative Review.Microorganisms · 2025Review
- Herbal Insights: Exploring the Therapeutic Potential of Indian Dietary Herbs in Diabetic Cardiomyopathy Management.Current diabetes reviews · 2025Review
- Chronic hyperglycemia impairs anti-microbial function of macrophages in response to Mycobacterium tuberculosis infection.Immunologic research · 2024Article
- Unraveling the Cardiac Matrix: From Diabetes to Heart Failure, Exploring Pathways and Potential Medications.Biomedicines · 2024Review
- Therapeutic strategies targeting mechanisms of macrophages in diabetic heart disease.Cardiovascular diabetology · 2024Review
- Cardiac macrophage metabolism in health and disease.Trends in endocrinology and metabolism: TEM · 2024Review
- Aldose reductase is a potential therapeutic target for neurodegeneration.Chemico-biological interactions · 2024Review
- Understanding Diabetic Cardiomyopathy: Insulin Resistance and Beyond.Heart international · 2024Review
- Association between METS-IR and heart failure: a cross-sectional study.Frontiers in endocrinology · 2024Article
- Ferroptosis: A New Mechanism in Diabetic Cardiomyopathy.International journal of medical sciences · 2024Review
- Hydrogen sulfide ameliorates senescence in vascular endothelial cells through ameliorating inflammation and activating PPARδ/SGLT2/STAT3 signaling pathway.Acta biochimica et biophysica Sinica · 2023Article
- The Aldose Reductase Inhibitor Epalrestat Maintains Blood-Brain Barrier Integrity by Enhancing Endothelial Cell Function during Cerebral Ischemia.Molecular neurobiology · 2023Article
- 2'-Hydroxy-4',5'-dimethoxyacetophenone Exhibit Collagenase, Aldose Reductase Inhibition, and Anticancer Activity Against Human Leukemic Cells: An In Vitro, and In Silico Study.Molecular biotechnology · 2023Article
- Roles of TSP1-CD47 signaling pathway in senescence of endothelial cells: cell cycle, inflammation and metabolism.Molecular biology reports · 2023Review
- Mechanisms of cardiac dysfunction in diabetic cardiomyopathy: molecular abnormalities and phenotypical variants.Heart failure reviews · 2023Review
- The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications.Frontiers in endocrinology · 2023Review
- The Significance of NLRP Inflammasome in Neuropsychiatric Disorders.Brain sciences · 2022Review
- Pyrroloquinoline quinone ameliorates diabetic cardiomyopathy by inhibiting the pyroptosis signaling pathway in C57BL/6 mice and AC16 cells.European journal of nutrition · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Despite recent studies that show oxidative stress-generated reactive oxygen species (ROS) regulate NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated innate immune response in various diabetic complications, the mechanism by which ROS activate innate immune response is not well understood. We have shown previously that aldose reductase (AR), besides reducing glucose, reduces lipid aldehydes and their glutathione conjugates and participates in various oxidative stress-induced inflammatory pathways. To understand the role of AR in ROS-induced innate immune response, we have investigated the mechanism(s) by which AR activates hyperglycemia-induced NLRP3 inflammsome-initiated innate immune response in Thp1 monocytes and in streptozotocin (STZ)-induced diabetic mice. In Thp1 monocytes, inhibition or ablation of AR prevented high-glucose-induced activation of NLRP3 inflammasome and caspase-1 and release of the innate immune cytokines interleukin (IL)-1β and IL-18. AR inhibition in Thp1 cells also prevented the high-glucose-induced generation of ROS, influx of Ca2+, efflux of K+, and activation of Lyn, Syk, and PI3K. Furthermore, the AR inhibitor fidarestat prevented the expression of NLRP inflammasome components in STZ-induced diabetic mouse heart and aorta, and also prevented the release of various cytokines in the serum. Collectively, our data suggest that AR regulates hyperglycemia-induced NLRP3 inflammasome-mediated innate immune response by altering the ROS/Lyn/Syk/PI3K/Ca2+/K+ signals.
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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.