ReviewJournal of molecular and cellular cardiology2021
MyD88: At the heart of inflammatory signaling and cardiovascular disease.
Review in Journal of molecular and cellular cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 100 citations in OpenAlex.
- Spinal neuronal TLR4-induced enhancement of nociceptive signals contributes to myocardial ischemia/reperfusion injury.Basic research in cardiology · 2026Article
- Identification MYD88 as a candidate molecule of sodium overload-induced cell death in myocardial ischemia-reperfusion injury.Journal of cardiothoracic surgery · 2026Article
- Intranasal MyD88-adjuvanted DNA vaccine against P. gingivalis in rat periodontitis.BMC oral health · 2026Article
- High mobility group box 1: DAMPening the danger molecule in cardiovascular disease with exercise.Cell stress & chaperones · 2026Review
- miR-138-5p Promotes HF in Rats by Reducing Histone Methylation in the Myd88 Promoter Region through Inhibition of EZH2.Acta Cardiologica Sinica · 2026Article
- Identification of key hub genes in spinal cord ischemia-reperfusion injury via integrated bioinformatics analysis and in vivo validation.Scientific reports · 2026Article
- Serial Expression of Pro-Inflammatory Biomarkers in Acute Lung Injury During the Post-Resuscitation Periods in Rats with Cardiac Arrest.International journal of molecular sciences · 2026Article
- Fisetin Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Targeting Myeloid Differentiation Factor 88.Inflammation · 2026Article
- Beyond receptor activation: biased toll-like receptor signaling in periodontal inflammation and regeneration.Frontiers in immunology · 2026Review
- Combined Nivolumab and Ipilimumab Therapy Promotes Immune-Mediated Cardiomyocyte Apoptosis Through TLR4-Myd88-NF-Human mutation · 2026Article
- Impact of High-Fat Diet on Biochemical Changes Following Experimental Myocardial Infarction.Journal of cellular and molecular medicine · 2025Article
- Alpinetin Alleviates Cardiac Inflammation and Remodeling via TLR4/MyD88/NF-κB Signaling Pathway in Rats with Acute Myocardial Infarction.International journal of molecular sciences · 2025Article
- USP7 Stabilizes USF1 to Aggravate ox-LDL-Induced Endothelial Injury Through the MYD88/NF-κB Pathway in Atherosclerosis.Applied biochemistry and biotechnology · 2025Article
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Geometrically controlled cardiac microtissues promote vascularization and reduce inflammationCell biomaterials · 2025Article
- G-quadruplex and i-motif DNA structures form in the promoter of the key innate immune adaptorCell reports. Physical science · 2025Article
- An examination of the LPS-TLR4 immune response through the analysis of molecular structures and protein-protein interactions.Cell communication and signaling : CCS · 2025Review
- MyD88 determines T cell fate through BCAP-PI3K signaling.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Atherosclerosis: A Comprehensive Review of Molecular Factors and Mechanisms.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiovascular disease is a leading cause of death worldwide and is associated with systemic inflammation. In depth study of the cell-specific signaling mechanisms mediating the inflammatory response is vital to improving anti-inflammatory therapies that reduce mortality and morbidity. Cellular damage in the cardiovascular system results in the release of damage associated molecular patterns (DAMPs), also known as "alarmins," which activate myeloid cells through the adaptor protein myeloid differentiation primary response 88 (MyD88). MyD88 is broadly expressed in most cell types of the immune and cardiovascular systems, and its role often differs in a cardiovascular disease context and cell specific manner. Herein we review what is known about MyD88 in the setting of a variety of cardiovascular diseases, discussing cell specific functions and the relative contributions of MyD88-dependent vs. independent alarmin triggered inflammatory signaling. The widespread involvement of these pathways in cardiovascular disease, and their largely unexplored complexity, sets the stage for future in depth mechanistic studies that may place MyD88 in both immune and non-immune cell types as an attractive target for therapeutic intervention in cardiovascular disease.
Indexed as
Identifiers
What 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.