ArticleCardiovascular research2023
Macrophage angiotensin-converting enzyme reduces atherosclerosis by increasing peroxisome proliferator-activated receptor α and fundamentally changing lipid metabolism.
Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.
What it found
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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.
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Who cites it
36 citing papers in PubMed, 48 citations in OpenAlex.
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- Myeloid cell renin-angiotensin-aldosterone system in hypertension and inflammation.Current opinion in physiology · 2026Article
- Targeted Metabolomics Uncovers NorCA's Role as a Potent Immunomodulator in Acute Pancreatitis by Promoting Macrophage Reprogramming and Efferocytosis.International journal of molecular sciences · 2026Article
- Macrophage efferocytosis promotes inflammation resolution and accelerates wound healing.Communications biology · 2026Review
- Bioengineered iPSC-derived human macrophages with increased angiotensin-converting enzyme (ACE) expression suppress solid tumor growth.Signal transduction and targeted therapy · 2026Article
- Fitness Training for γδ T cells in mouse and human atherosclerosis takes place in plaques and artery tertiary lymphoid organs.Genome medicine · 2026Article
- Splenic cDC1 efferocytosis and cross-presentation to CD8 T cells are promoted by GPR34 and lysophosphatidylserine.The Journal of experimental medicine · 2026Article
- Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity.Frontiers in immunology · 2026Review
- Investigating Alternative Treatments for Dyslipidemia Using Bioactive Compounds Derived from Kiwifruit (Actinidia chinensis): A Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulation Analysis.Current drug targets · 2026Article
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Protein palmitoylation in hematological malignancies: mechanistic links to lipid metabolic reprogramming and therapy resistance.Frontiers in immunology · 2026Review
- Immune and metabolic remodeling following bariatric surgery: Implications for targeted immunotherapy (Review).International journal of molecular medicine · 2026Review
- PCSK9 inhibition alleviates sepsis-induced myocardial dysfunction by facilitating PINK1/parkin-associated mitophagy.Frontiers in pharmacology · 2026Article
- The functional role of exosomalTranslational cancer research · 2025Article
- ELABELA Ameliorates Atherosclerosis Through Restoring the M1/M2 Macrophage Balance inJournal of the American Heart Association · 2025Article
- Alzheimer's disease pathogenesis: standing at the crossroad of lipid metabolism and immune response.Molecular neurodegeneration · 2025Review
- Targeting Splenic Myeloid Cells with Nanobiologics to Prevent Postablative Pancreatic Cancer Recurrence via Inducing Antitumor Peripheral Trained Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- USP22 enhances atherosclerotic plaque stability and macrophage efferocytosis by stabilizing PPARγ.Communications biology · 2025Article
- Fueling defense: PPARα enhances macrophage inflammatory responses.Cellular & molecular immunology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
aimsThe metabolic failure of macrophages to adequately process lipid is central to the aetiology of atherosclerosis. Here, we examine the role of macrophage angiotensin-converting enzyme (ACE) in a mouse model of PCSK9-induced atherosclerosis. METHODS AND
resultsAtherosclerosis in mice was induced with AAV-PCSK9 and a high-fat diet. Animals with increased macrophage ACE (ACE 10/10 mice) have a marked reduction in atherosclerosis vs. WT mice. Macrophages from both the aorta and peritoneum of ACE 10/10 express increased PPARα and have a profoundly altered phenotype to process lipids characterized by higher levels of the surface scavenger receptor CD36, increased uptake of lipid, increased capacity to transport long chain fatty acids into mitochondria, higher oxidative metabolism and lipid β-oxidation as determined using 13C isotope tracing, increased cell ATP, increased capacity for efferocytosis, increased concentrations of the lipid transporters ABCA1 and ABCG1, and increased cholesterol efflux. These effects are mostly independent of angiotensin II. Human THP-1 cells, when modified to express more ACE, increase expression of PPARα, increase cell ATP and acetyl-CoA, and increase cell efferocytosis.
conclusionIncreased macrophage ACE expression enhances macrophage lipid metabolism, cholesterol efflux, efferocytosis, and it reduces atherosclerosis. This has implications for the treatment of cardiovascular disease with angiotensin II receptor antagonists vs. ACE inhibitors.
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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.