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TLR4 stands at the forefront of innate immune responses, recognizing various pathogen- associated molecular patterns and endogenous ligands, thus serving as a pivotal mediator in the immune system's defense against infections and tissue damage. Beyond its canonical role in infection, emerging evidence highlights TLR4's involvement in numerous non-infectious human diseases, ranging from metabolic disorders to neurodegenerative conditions and cancer. Targeting TLR4 signaling pathways presents a promising therapeutic approach with broad applicability across these diverse pathological states. In metabolic disorders such as obesity and diabetes, dysregulated TLR4 activation contributes to chronic low-grade inflammation and insulin resistance, driving disease progression. In cardiovascular diseases, TLR4 signaling promotes vascular inflammation and atherogenesis, implicating its potential as a therapeutic target to mitigate cardiovascular risk. Neurodegenerative disorders, including Alzheimer's and Parkinson's diseases, exhibit aberrant TLR4 activation linked to neuroinflammation and neuronal damage, suggesting TLR4 modulation as a strategy to attenuate neurodegeneration. Additionally, in cancer, TLR4 signaling within the tumor microenvironment promotes tumor progression, metastasis, and immune evasion, underscoring its relevance as a target for anticancer therapy. Advances in understanding TLR4 signaling cascades and their contributions to disease pathogenesis have spurred the development of various pharmacological agents targeting TLR4. These agents range from small molecule inhibitors to monoclonal antibodies, with some undergoing preclinical and clinical evaluations. Furthermore, strategies involving TLR4 modulation through dietary interventions and microbiota manipulation offer additional avenues for therapeutic exploration. Hence, targeting TLR4 holds significant promise as a therapeutic strategy across a spectrum of human diseases, offering the potential to modulate inflammation, restore immune homeostasis, and impede disease progression.
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http://dx.doi.org/10.2174/0113892037324425241018061548 | DOI Listing |
Drug Des Devel Ther
September 2025
Department of Neurosurgery, Peking University People's Hospital, Beijing, People's Republic of China.
Introduction: Parkinson's disease (PD) is a neurodegenerative disorder lacking therapies to replace lost dopaminergic neurons. Neural stem cell (NSC) transplantation faces survival and differentiation challenges. This study investigated feasibility and efficacy of paeoniflorin (PF) combined with NSC transplantation for PD treatment.
View Article and Find Full Text PDFEur J Clin Pharmacol
September 2025
Department of Clinical Pharmacy, Faculty of Pharmacy, Tanta University, Tanta, Egypt.
Objective: This research aimed at evaluating the effectiveness and safety of nitazoxanide and escitalopram as adjuvant therapies in patients with rheumatoid arthritis (RA).
Methods: In this randomized controlled parallel study, 90 patients with active RA were randomized into three groups; group 1 (control group; n = 30) which received traditional therapy, group 2 (Nitazoxanide group; n = 30) which received traditional therapy plus 1 gm/day oral nitazoxanide, and group 3 (Escitalopram group; n = 30) which received traditional therapy plus 10 mg/day oral escitalopram for three months. At baseline and 3 months after treatment, clinical and functional assessments were done through the 28-joint count disease activity score using C-reactive protein (DAS28-CRP), the health assessment questionnaire-disability index (HAQ-DI), and the patient's global assessment (PGA).
Am J Transplant
September 2025
Center for Transplantation Sciences, Massachusetts General Hospital, Harvard Medical School; Department of Surgery, Massachusetts General Hospital, Harvard Medical School; Department of Surgery, Hospital of the University of Pennsylvania, Perelman School of Medicine at the University of Pennsylvania
Achieving immune tolerance is a key goal in organ transplantation, as it eliminates the need for long-term immunosuppression. Regulatory B cells (Bregs) present a promising strategy for inducing tolerance. Our previous findings demonstrate that the adoptive transfer of ex vivo-expanded murine splenic B regulatory cells, referred to as TLR-Bregs (TLR9/TLR4 stimulation), induces tolerance to allografts.
View Article and Find Full Text PDFChem Biodivers
September 2025
School of Pharmaceutical Science, Yunnan Key Laboratory of Pharmacology for Natural Products/College of Modern Biomedical Industry, NHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, P. R. China.
20(R)-ginsenoside Rg3 can reduce the effects of oxidative stress and cell death in cerebral ischemia‒reperfusion injury (CIRI). Neuroinflammation is crucial post-CIRI, but how 20(R)-Rg3 affects ischemia‒reperfusion-induced neuroinflammation is unclear. To study 20(R)-Rg3's effects on neuroinflammation and neuronal preservation in stroke models and explore toll-like receptor 4/myeloid differentiation factor-88/nuclear factor kappa B (TLR4/MyD88/NF-κB) pathway mechanisms.
View Article and Find Full Text PDFCardiovasc Res
September 2025
Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University in Saint Louis, St. Louis, MO, USA.
Aims: Although the ability of the heart to adapt to environmental stress has been studied extensively, the molecular and cellular mechanisms responsible for cardioprotection are not yet fully understood. In this study, we sought to elucidate these mechanisms for cytoprotection using a model of stress-induced cardiomyopathy.
Methods And Results: We administered Toll-like receptor (TLR) agonists or diluent to wild-type mice and assessed for cardioprotection against injury from a high intraperitoneal dose of isoproterenol (ISO) administered 7 days later.