ReviewAnnual review of pharmacology and toxicology2011
Macrophages and tissue injury: agents of defense or destruction?
Review in Annual review of pharmacology and toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 301 papers, 2 of them syntheses that pooled it.
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
301 citing papers in PubMed, 2 syntheses or guidelines pooled it, 593 citations in OpenAlex.
- Autoimmunity and hernia mesh: fact or fiction?Hernia : the journal of hernias and abdominal wall surgery · 2023Pooled it
- A Barrier to Defend - Models of Pulmonary Barrier to Study Acute Inflammatory Diseases.Frontiers in immunology · 2022Pooled it
- Exosomes derived from M1-macrophage promote enteric neuronal injury via MMP8-TGF-β pathway.Journal of advanced research · 2026Article
- [Dietary serine supplementation inhibits the hepatic macrophage AKT/mTOR pathway and improves primary biliary cholangitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Article
- Fine particulate matter and tobacco product exposure exacerbates metabolic syndrome-related colon cancer via regulating oxidative stress and tumor-associated macrophage interactions.Cancer & metabolism · 2026Article
- Exosomal lncRNA OTUD6B-AS1 as a pathogenic nanocarrier promotes inflammatory macrophage polarization in endometritis via a targetable ceRNA circuit.Materials today. Bio · 2026Article
- Cell-based drug delivery for combating bacteria: focus on refractory infections.Journal of nanobiotechnology · 2026Review
- Article
- Chromium(VI) Modulates Macrophage Polarization and Metabolic Reprogramming to Impair Immune Function.Toxics · 2026Article
- Alisol F 24-acetate attenuated metabolic dysfunction-associated steatohepatitis by targeting the KEAP1/NRF2-mediated macrophage pyroptosis.Chinese medicine · 2026Article
- Differential expression of apoptosis markers in early-phase sulfur mustard-induced pulmonary injuries.Journal of molecular histology · 2026Article
- Sphingosine-1-phosphate receptor signaling regulates an ERK1/2-p65 molecular switch in macrophages duringFrontiers in pharmacology · 2026Article
- How Cytokines Regulate Immune Response Toward Chronic Allograft Rejection?Results and problems in cell differentiation · 2026Review
- IL-17A-Induced Redox Imbalance and Inflammatory Responses in Mice Lung via Act1-TRAF6-IKBα Signaling Pathway: Implications for Lung Disease Pathogenesis.Inflammation · 2025Article
- Macrophages: Subtypes, Distribution, Polarization, Immunomodulatory Functions, and Therapeutics.MedComm · 2025Review
- Roles of circadian clocks in macrophage metabolism: implications in inflammation and metabolism of lipids, glucose, and amino acids.American journal of physiology. Endocrinology and metabolism · 2025Review
- Tumor-Associated Macrophages as Key Modulators of Disease Progression in Diffuse Large B-Cell Lymphoma.Biomedicines · 2025Review
- Effects of aged garlic extract on macrophage functions: a short review of experimental evidence (Review).Biomedical reports · 2025Review
- Inhibitory effects of AptaminC320 targeting vitamin C on LPS-induced inflammation in RAW264.7 cells.Biochemistry and biophysics reports · 2025Article
- Article
241 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The past several years have seen the accumulation of evidence demonstrating that tissue injury induced by diverse toxicants is due not only to their direct effects on target tissues but also indirectly to the actions of resident and infiltrating macrophages. These cells release an array of mediators with cytotoxic, pro- and anti-inflammatory, angiogenic, fibrogenic, and mitogenic activity, which function to fight infections, limit tissue injury, and promote wound healing. However, following exposure to toxicants, macrophages can become hyperresponsive, resulting in uncontrolled or dysregulated release of mediators that exacerbate acute tissue injury and/or promote the development of chronic diseases such as fibrosis and cancer. Evidence suggests that the diverse activity of macrophages is mediated by distinct subpopulations that develop in response to signals within their microenvironment. Understanding the precise roles of these different macrophage populations in the pathogenic response to toxicants is key to designing effective treatments for minimizing tissue damage and chronic disease and for facilitating wound repair.
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.