ArticleDiabetes2016
Toll-Like Receptor 4 Activation Contributes to Diabetic Bladder Dysfunction in a Murine Model of Type 1 Diabetes.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 51 citations in OpenAlex.
- Effect of Bladder Injections of Botulinum Neurotoxin A on Biomarkers Associated with Inflammation and Urinary Infections in Patients with Neurogenic Detrusor Overactivity-Associated Incontinence: A Pilot, Prospective, Human Study.International journal of molecular sciences · 2026Article
- TLR4 deletion reduces small fiber sensory abnormalities and nerve degeneration in diabetic male mice.Neuroscience · 2025Article
- Association between early age at menarche and overactive bladder risk in women: insights from NHANES and Mendelian randomization analysis.Translational andrology and urology · 2025Article
- Impact of excessive hypercholesterolemia in pregnancy on the placentas of the male and female offspring.Scientific reports · 2025Article
- Article
- Construction of a management protocol for high-risk neurogenic bladder in Chinese patients with type 2 diabetes: a Delphi study.Frontiers in endocrinology · 2025Article
- Exploring the therapeutic effects of sulforaphane: an in-depth review on endoplasmic reticulum stress modulation across different disease contexts.Inflammopharmacology · 2024Review
- Interaction of Pexiganan (MSI-78)-Derived Analogues Reduces Inflammation and TLR4-Mediated Cytokine Secretion: A Comparative Study.ACS omega · 2023Article
- Established and emerging treatments for diabetes-associated lower urinary tract dysfunction.Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Chrysin ameliorates STZ-induced diabetes in rats: possible impact of modulation of TLR4/NF-κβ pathway.Research in pharmaceutical sciences · 2022Article
- Inflammation triggered by the NLRP3 inflammasome is a critical driver of diabetic bladder dysfunction.Frontiers in physiology · 2022Review
- Mechanisms of altered bone remodeling in children with type 1 diabetes.World journal of diabetes · 2021Review
- Role of TLR4/MyD88/NF-κB signaling in heart and liver-related complications in a rat model of type 2 diabetes mellitus.The Journal of international medical research · 2021Article
- Antagonism of proNGF or its receptor p75Diabetologia · 2020Article
- Metabolic abnormalities exacerbate Sjögren's syndrome by and is associated with increased the population of interleukin-17-producing cells in NOD/ShiLtJ mice.Journal of translational medicine · 2020Article
- Review
- Toll-like receptor 9 regulates metabolic profile and contributes to obesity-induced benign prostatic hyperplasia in mice.Pharmacological reports : PR · 2020Article
- Smooth muscle-specific deletion of MnSOD exacerbates diabetes-induced bladder dysfunction in mice.American journal of physiology. Renal physiology · 2019Article
- Relationship between alterations of urinary microbiota and cultured negative lower urinary tract symptoms in female type 2 diabetes patients.BMC urology · 2019Article
- Detrusor contractility to parasympathetic mediators is differentially altered in the compensated and decompensated states of diabetic bladder dysfunction.American journal of physiology. Renal physiology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Diabetic bladder dysfunction (DBD) is a common urological complication of diabetes. Innate immune system activation via Toll-like receptor 4 (TLR4) leads to inflammation and oxidative stress and was implicated in diabetes pathophysiology. We hypothesized that bladder hypertrophy and hypercontractility in DBD is mediated by TLR4 activation. Wild-type (WT) and TLR4 knockout (TLR4KO) mice were made diabetic by streptozotocin (STZ) treatment, and bladder contractile function and TLR4 pathway expression were evaluated. Immunohistochemistry confirmed the expression of TLR4 in human and mouse bladder. Recombinant high-mobility group box protein 1 (HMGB1) increased bladder TLR4 and MyD88 expression and enhanced contractile response to electrical field stimulation. Bladder expression of TLR4 and MyD88 and serum expression of HMGB1 were increased in STZ compared with control mice. Carbachol (CCh)-mediated contraction was increased in bladders from STZ mice, and TLR4 inhibitor CLI-095 attenuated this increase. Induction of diabetes by STZ in WT mice increased bladder weight and contractile responses to CCh and to electrical field stimulation. TLR4KO mice were not protected from STZ-induced diabetes; however, despite levels of hyperglycemia similar to those of WT STZ mice, TLR4KO STZ mice were protected from diabetes-induced bladder hypertrophy and hypercontractility. These data suggest that TLR4 activation during diabetes mediates DBD-associated bladder hypertrophy and hypercontractility.
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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.