ArticleNature communications2024
Lipid synthesis, triggered by PPARγ T166 dephosphorylation, sustains reparative function of macrophages during tissue repair.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
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- α-Ketoglutarate accelerates cutaneous wound healing through modulating the epithelial-fibroblast niche.JCI insight · 2026Article
- Regulating xenophagy and phenotype of macrophages by selenium-doped nanoleaves on Zn-based implants for infected bone integration.Bioactive materials · 2026Article
- Mechano-reprogramming of tumor-associated macrophages by engineering nanogel stiffness for suppression of tumor development.Journal of nanobiotechnology · 2026Article
- Uremic toxins promote renal fatty acid synthesis and fibrosis via activating aryl hydrocarbon receptor.Nature communications · 2026Article
- SAMHD1 promotes cardiac repair post myocardial infarction by targeting NR4a1 to regulate macrophage metabolic reprogramming.Journal of advanced research · 2026Article
- Dynamic remodeling of amino acid metabolism in tumor-associated macrophages: Fueling immunosuppression, reshaping tumor niches, and unlocking metabolic checkpoints.Journal of advanced research · 2026Review
- Phenyllactic Acid Restores Intestinal Epithelial Barrier to Alleviate Hypertriglyceridemic Acute Pancreatitis via a PPARγ-Dependent Mechanism.Antioxidants (Basel, Switzerland) · 2026Article
- Metabolic pattern changes of macrophages during cancer development and progression.Journal of translational medicine · 2026Review
- Volumetric absorptive microsampling for profiling of signaling lipids: a comparative analysis with whole blood and dried blood spots.Analytical and bioanalytical chemistry · 2026Article
- Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026Review
- Development and validation of a prognosis model for low-grade gliomas based on metabolic gene risk scoring and immune microenvironment interaction.Discover oncology · 2026Article
- IL-33-Driven Macrophage Reprogramming as a Potential Immunometabolic Strategy for Herpes Simplex Keratitis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
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- Bicaudal‑C1 in Cancer: Molecular Mechanisms and Therapeutic Strategies Integrating Chinese and Western Medicine.Drug design, development and therapy · 2026Review
- Integrated Bulk and Single-Cell Transcriptomics Reveals Cell-Type-Specific Fatty Acid Metabolic Dysregulation and Candidate Biomarkers in Diabetic Foot Ulcers.Clinical, cosmetic and investigational dermatology · 2026Article
- The Mechanistic Role of PPARPPAR research · 2026Review
- Integrated Network Pharmacology Analysis and Experimental Validation of Zadi-5 Against Coronary Heart Disease.Cardiology research and practice · 2026Article
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Authors and funding
13 authors.
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Abstract
Macrophages may acquire a reparative phenotype that supports tissue repair and remodeling in response to tissue injury. However, the metabolic requirements underpinning this process are incompletely understood. Here, we show that posttranslational modification (PTM) of PPARγ regulates lipid synthesis in response to wound microenvironmental cues and that metabolic rewiring orchestrates function of reparative macrophages. In injured tissues, repair signaling leads to decreased macrophage PPARγ threonine 166 (T166) phosphorylation, which results in a partially active PPARγ transcriptional program comprised of increased binding activity to the regulator regions of lipid synthesis-associated genes, thereby increased lipogenesis. The accumulated lipids serve as signaling molecules, triggering STAT3-mediated growth factor expression, and supporting the synthesis of phospholipids for the expansion of the endoplasmic reticulum (ER), which is required for protein secretion. Genetic or pharmacological inhibition of PPARγ T166 phosphorylation promotes the reparative function of macrophages and facilitates tissue regeneration. In summary, our work identifies PPARγ T166-regulated lipid biosynthesis as an essential pathway for meeting the anabolic demands of the activation and function of macrophages and provides a rationale for potential therapeutic targeting of tissue repair.
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