ArticleJournal of translational autoimmunity2024
ANKRD22 aggravates sepsis-induced ARDS and promotes pulmonary M1 macrophage polarization.
Article in Journal of translational autoimmunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- A systematic review of protein post-translational modifications in sepsis.Molecular biology reports · 2025Pooled it
- Monocyte-Amplified Transcriptional Signatures of Human Diseases.bioRxiv : the preprint server for biology · 2026Article
- Downregulation of ANKRD22 promotes ovarian cancer cell proliferation by enhancing the immunosuppressive capacity of M-MDSCs.Cancer immunology, immunotherapy : CII · 2026Article
- ProBDNF promotes LPS-induced pro-inflammatory polarization of alveolar macrophages via the Notch1 signaling pathway.Immunologic research · 2026Article
- Targeted silencing of CLYBL with platelet-mimetic siRNA nanoparticles drives itaconate-mediated macrophage reprogramming and protects against sepsis-triggered lung cell death.Cell death discovery · 2026Article
- Mechanisms and therapeutics of immunometabolic reprogramming driving macrophage-ECs interactions in sepsis-associated ARDS from the gut-lung axis perspective.Frontiers in immunology · 2026Review
- Lipoxin A4 AttenuatesJournal of inflammation research · 2026Article
- Hepatocyte-Specific GSDMD Deficiency Aggravates Sepsis by Disrupting Non-Canonical Secretion of Anti-Inflammatory Factors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Anti-inflammatory effect of nestorone in a lipopolysaccharide-induced acute lung injury model through regulation of the TLR-4/Myd88/NF-κB signaling pathway.Inflammopharmacology · 2025Article
- The role of natural products targeting macrophage polarization in sepsis-induced lung injury.Chinese medicine · 2025Review
- ANKRD22 participates in the proinflammatory activities of macrophages in the colon cancer tumor microenvironment.Cancer immunology, immunotherapy : CII · 2025Article
- Identification of amino acid metabolism‑related genes as diagnostic and prognostic biomarkers in sepsis through machine learning.Experimental and therapeutic medicine · 2025Article
- From "metabolic storm" to "immune paralysis": the dynamic evolution of macrophages and metabolism reprogramming in ARDS.Frontiers in immunology · 2025Review
- Macrophages in sepsis-induced acute lung injury: exosomal modulation and therapeutic potential.Frontiers in immunology · 2024Review
- The impact of glucose metabolism on inflammatory processes in sepsis-induced acute lung injury.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute respiratory distress syndrome (ARDS) is independently associated with a poor prognosis in patients with sepsis. Macrophage M1 polarization plays an instrumental role in this process. Therefore, the exploration of key molecules affecting acute lung injury and macrophage M1 polarization may provide therapeutic targets for the treatment of septic ARDS. Here, we identified that elevated levels of Ankyrin repeat domain-containing protein 22 (ANKRD22) were associated with poor prognosis and more pronounced M1 macrophage polarization in septic patients by analyzing high-throughput data. ANKRD22 expression was also significantly upregulated in the alveolar lavage fluid, peripheral blood, and lung tissue of septic ARDS model mice. Knockdown of ANKRD22 significantly attenuated acute lung injury in mice with sepsis-induced ARDS and reduced the M1 polarization of lung macrophages. Furthermore, deletion of ANKRD22 in macrophages inhibited M1 macrophage polarization and reduced levels of phosphorylated IRF3 and intracellular interferon regulatory factor 3 (IRF3) expression, while re-expression of ANKRD22 reversed these changes. Further experiments revealed that ANKRD22 promotes IRF3 activation by binding to mitochondrial antiviral-signaling protein (MAVS). In conclusion, these findings suggest that ANKRD22 promotes the M1 polarization of lung macrophages and exacerbates sepsis-induced ARDS.
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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.