ArticleFrontiers in immunology2017
Toll-Like Receptor 4 Inhibition Improves Oxidative Stress and Mitochondrial Health in Isoproterenol-Induced Cardiac Hypertrophy in Rats.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 64 citations in OpenAlex.
- Isoproterenol-induced cardiac hypertrophy: mechanistic insights, environmental stressor and molecular cardioprotection.Molecular biology reports · 2026Review
- The Gut Microbiome in Heart Failure: Pathways to Inflammation and Therapeutic Targets.Metabolites · 2026Review
- HMGB1 and mitochondrial dysfunction: a double-edged sword in ageing.Open biology · 2025Review
- TLR4 deficiency does not alter glaucomatous progression in a mouse model of chronic glaucoma.Scientific reports · 2025Article
- Peripheral immune cell response to stimulation stratifies Parkinson's disease progression from prodromal to clinical stages.Communications biology · 2025Article
- Goutweed (Molecules (Basel, Switzerland) · 2025Review
- Cell autonomous TLR4 signaling modulates TGF-β induced activation of human cardiac fibroblasts.Heliyon · 2025Article
- Ceftriaxone and MC-100093 mitigate fentanyl-induced cardiac injury in mice: Preclinical investigation of its underlying molecular mechanisms.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Article
- Review
- Cardiomyocyte-specific deletion of TLR4 attenuates angiotensin II-induced hypertension and cardiac remodeling.Frontiers in cardiovascular medicine · 2023Article
- Toll-like receptors in cardiac hypertrophy.Frontiers in cardiovascular medicine · 2023Review
- Sexually dimorphic effects of SARM1 deletion on cardiac NADAmerican journal of physiology. Heart and circulatory physiology · 2022Article
- Anti-Diabetic Therapy, Heart Failure and Oxidative Stress: An Update.Journal of clinical medicine · 2022Review
- Venetoclax Induces Cardiotoxicity through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway.International journal of molecular sciences · 2022Article
- Nutraceutical, Dietary, and Lifestyle Options for Prevention and Treatment of Ventricular Hypertrophy and Heart Failure.International journal of molecular sciences · 2021Review
- Activation of toll like receptor 4 (TLR4) promotes cardiomyocyte apoptosis through SIRT2 dependent p53 deacetylation.Scientific reports · 2020Article
- Long non-coding RNAs in cardiac hypertrophy.Heart failure reviews · 2020Review
- Mitochondrial Dysfunction in Diabetic Cardiomyopathy: The Possible Therapeutic Roles of Phenolic Acids.International journal of molecular sciences · 2020Review
- Plants as Sources of Anti-Inflammatory Agents.Molecules (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammation remains a crucial factor for progression of cardiac diseases and cardiac hypertrophy remains an important cause of cardiac failure over all age groups. As a key regulator of inflammation, toll-like receptor 4 (TLR4) plays an important role in pathogenesis of cardiac diseases. Being an important regulator of innate immunity, the precise pathway of TLR4-mediated cardiac complications is yet to be established. Therefore, the primary objective of the present study was to find the role of TLR4 in cardiac hypertrophy and the molecular mechanism thereof.
methodsCardiac hypertrophy was induced with administration of isoproterenol (5 mg/kg/day, sc). TLR4 receptor inhibitor RS-LPS (lipopolysaccharide from the photosynthetic bacterium
resultsCardiac hypertrophy was confirmed with increased heart weight/body weight ratio as well as assessment of hypertrophic markers in heart. There was a marked increase in the TLR4 expression and oxidative stress along with mitochondrial dysfunction in ISO group. TLR4 inhibition significantly decreased heart weight/body weight ratio and ANP, collagen, and β-MHC expression and restored the disturbed cellular antioxidant flux. The mitochondrial perturbations that were observed in hypertrophy heart was normalized after administration of TLR4 inhibitor but not with the agonist. TLR4 agonism further exaggerated the oxidative stress in heart and hence accelerated the disease development and progression.
conclusionOur data show that increased TLR4 ligand pool in cardiac hypertrophy may exaggerate the disease progression. However, inhibition of TLR4 attenuated cardiac hypertrophy through reduced cardiac redox imbalance and mitochondrial dysfunction.
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