ArticleMolecular therapy. Nucleic acids2023
Inhibition of pro-inflammatory signaling in human primary macrophages by enhancing arginase-2 via target site blockers.
Article in Molecular therapy. Nucleic acids, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 4 citations in OpenAlex.
- Timing-dependent anti-inflammatory effects of empagliflozin in monocyte-derived macrophages from post-myocardial infarct patients with type 2 diabetes.Cardiovascular diabetology · 2026Trial
- Macrophage Plasticity: Phenotypic and Functional Profiles Across Pathological Microenvironments.International journal of molecular sciences · 2026Review
- Macrophage metabolism reprogramming in sepsis: Pathogenesis and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Extracellular vesicles derived from induced pluripotent stem cells mediate anti-inflammatory effects in primary human macrophages.Scientific reports · 2026Article
- Article
- Organosulfur compounds as dual-action agents: a critical review of antimicrobial and immunomodulatory potentials, and translational barriers.Frontiers in pharmacology · 2026Review
- Arginine metabolism in myeloid cells in health and disease.Seminars in immunopathology · 2025Review
- X-inactive specific transcript (XIST) can determine sex differences in cardiovascular drug responses: focus on RNA therapeutics.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The modulation of macrophage phenotype from a pro-inflammatory to an anti-inflammatory state holds therapeutic potential in the treatment of inflammatory disease. We have previously shown that arginase-2 (Arg2), a mitochondrial enzyme, is a key regulator of the macrophage anti-inflammatory response. Here, we investigate the therapeutic potential of Arg2 enhancement via target site blockers (TSBs) in human macrophages. TSBs are locked nucleic acid antisense oligonucleotides that were specifically designed to protect specific microRNA recognition elements (MREs) in human
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