ArticleMolecular and cellular therapies2015
Cross talk of the first-line defense TLRs with PI3K/Akt pathway, in preconditioning therapeutic approach.
Article in Molecular and cellular therapies, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 48 citations in OpenAlex.
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- Calreticulin in the nasal mucus promotes neutrophil migration and pathogen clearance.Cell communication and signaling : CCS · 2025Article
- Cytoprotective Effects ofAntioxidants (Basel, Switzerland) · 2025Article
- Article
- Mesenchymal Stem Cells Regulate Microglial Polarization via Inhibition of the HMGB1/TLR4 Signaling Pathway in Diabetic Retinopathy.Inflammation · 2024Article
- Akt activator SC79 stimulates antibacterial nitric oxide generation in human nasal epithelial cells in vitro.International forum of allergy & rhinology · 2024Article
- Effects of Akt Activator SC79 on Human M0 Macrophage Phagocytosis and Cytokine Production.Cells · 2024Article
- Dichotomous roles of RIPK3 in regulating the IFN response and NLRP3 inflammasome in human monocytes.Journal of leukocyte biology · 2023Article
- Preventive effects of inotodiol on polyinosinic-polycytidylic acid-induced inflammation in human dermal fibroblasts.Heliyon · 2023Article
- Cells resident to precision templated 40-µm pore scaffolds generate small extracellular vesicles that affect CD4Acta biomaterialia · 2023Article
- Mitigation of acetaminophen-induced liver toxicity by the novel phosphatidylinositol 3-kinase inhibitor alpelisib.Frontiers in pharmacology · 2023Article
- PI3K signalling at the intersection of cardio-oncology networks: cardiac safety in the era of AI.Cellular and molecular life sciences : CMLS · 2022Review
- Dietary mannan oligosaccharides strengthens intestinal immune barrier functionFrontiers in immunology · 2022Article
- Substrate stiffness induces neutrophil extracellular trap (NET) formation through focal adhesion kinase activation.Biomaterials · 2021Article
- Mitochondria and Pharmacologic Cardiac Conditioning-At the Heart of Ischemic Injury.International journal of molecular sciences · 2021Review
- Poly(I:C) preconditioning protects the heart against myocardial ischemia/reperfusion injury through TLR3/PI3K/Akt-dependent pathway.Signal transduction and targeted therapy · 2020Article
- Targeting the phosphoinositide-3-kinase/protein kinase B pathway in airway innate immunity.World journal of biological chemistry · 2020Review
- TLR Agonists as Mediators of Trained Immunity: Mechanistic Insight and Immunotherapeutic Potential to Combat Infection.Frontiers in immunology · 2020Review
- Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4.Frontiers in cardiovascular medicine · 2020Review
- Extensive Changes in Transcriptomic "Fingerprints" and Immunological Cells in the Large Organs of Patients Dying of Acute Septic Shock and Multiple Organ Failure Caused byFrontiers in cellular and infection microbiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor family (TLRs), pattern recognition receptors, is expressed not only on immune cells but also on non-immune cells, including cardiomyocytes, fibroblasts, and vascular endothelial cells. One main function of TLRs in the non-immune system is to regulate apoptosis. TLRs are the central mediators in hepatic, pulmonary, brain, and renal ischemic/reperfusion (I/R) injury. Up-regulation of TLRs and their ligation by either exogenous or endogenous danger signals plays critical roles in ischemia/reperfusion-induced tissue damage. Conventional TLR-NF-κB pathways are markedly activated in failing and ischemic myocardium. Recent studies have identified a cross talk between TLR activation and the PI3K/Akt pathway. The activation of TLRs is proposed to be the most potent preconditioning method after ischemia, to improve the cell survival via the mechanism involved the PI3K/Akt signaling pathway and to attenuate the subsequent TLR-NF-κB pathway stimulation. Thus, TLRs could be a great target in the new treatment approaches for myocardial I/R injury.
Indexed as
Identifiers
26056605PMC4456045W2113242667What 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.