ArticleJournal of lipid research2014
Deletion of CGI-58 or adipose triglyceride lipase differently affects macrophage function and atherosclerosis.
Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Lipid droplets beyond storage: Cellular metabolic modulator in the diabetic heart (Review).International journal of molecular medicine · 2026Review
- Coordinated inhibition of M1 macrophage polarization by FIT2-mediated lipid droplet biosynthesis and FABP5.Zoological research · 2025Article
- Deficiency of Adipose Triglyceride Lipase Induces Metabolic Syndrome and Cardiomyopathy in Zebrafish.International journal of molecular sciences · 2022Article
- Review
- Triglyceride breakdown from lipid droplets regulates the inflammatory response in macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Association between the levels of CGI-58 and lipoprotein lipase in the placenta of patients with preeclampsia.Experimental and therapeutic medicine · 2021Article
- Elevated S-adenosylhomocysteine induces adipocyte dysfunction to promote alcohol-associated liver steatosis.Scientific reports · 2021Article
- CGI-58: Versatile Regulator of Intracellular Lipid Droplet Homeostasis.Advances in experimental medicine and biology · 2020Review
- The α/β-hydrolase domain-containing 4- and 5-related phospholipase Pummelig controls energy storage inJournal of lipid research · 2019Article
- Metformin protects against oxidized low density lipoprotein-induced macrophage apoptosis and inhibits lipid uptake.Experimental and therapeutic medicine · 2018Article
- Novel Pharmacological Probes Reveal ABHD5 as a Locus of Lipolysis Control in White and Brown Adipocytes.The Journal of pharmacology and experimental therapeutics · 2017Article
- Critical roles for α/β hydrolase domain 5 (ABHD5)/comparative gene identification-58 (CGI-58) at the lipid droplet interface and beyond.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Review
- Regulation of Hepatic Triacylglycerol Metabolism by CGI-58 Does Not Require ATGL Co-activation.Cell reports · 2016Article
- Macrophage ABHD5 promotes colorectal cancer growth by suppressing spermidine production by SRM.Nature communications · 2016Article
- Monoglyceride lipase deficiency modulates endocannabinoid signaling and improves plaque stability in ApoE-knockout mice.Atherosclerosis · 2016Article
- Adipose triglyceride lipase acts on neutrophil lipid droplets to regulate substrate availability for lipid mediator synthesis.Journal of leukocyte biology · 2015Article
- Active autophagy but not lipophagy in macrophages with defective lipolysis.Biochimica et biophysica acta · 2015Article
- Fatty Acid-binding Proteins Interact with Comparative Gene Identification-58 Linking Lipolysis with Lipid Ligand Shuttling.The Journal of biological chemistry · 2015Article
- Muscle-specific deletion of comparative gene identification-58 (CGI-58) causes muscle steatosis but improves insulin sensitivity in male mice.Endocrinology · 2015Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Cellular TG stores are efficiently hydrolyzed by adipose TG lipase (ATGL). Its coactivator comparative gene identification-58 (CGI-58) strongly increases ATGL-mediated TG catabolism in cell culture experiments. To investigate the consequences of CGI-58 deficiency in murine macrophages, we generated mice with a targeted deletion of CGI-58 in myeloid cells (macCGI-58(-/-) mice). CGI-58(-/-) macrophages accumulate intracellular TG-rich lipid droplets and have decreased phagocytic capacity, comparable to ATGL(-/-) macrophages. In contrast to ATGL(-/-) macrophages, however, CGI-58(-/-) macrophages have intact mitochondria and show no indications of mitochondrial apoptosis and endoplasmic reticulum stress, suggesting that TG accumulation per se lacks a significant role in processes leading to mitochondrial dysfunction. Another notable difference is the fact that CGI-58(-/-) macrophages adopt an M1-like phenotype in vitro. Finally, we investigated atherosclerosis susceptibility in macCGI-58/ApoE-double KO (DKO) animals. In response to high-fat/high-cholesterol diet feeding, DKO animals showed comparable plaque formation as observed in ApoE(-/-) mice. In agreement, antisense oligonucleotide-mediated knockdown of CGI-58 in LDL receptor(-/-) mice did not alter atherosclerosis burden in the aortic root. These results suggest that macrophage function and atherosclerosis susceptibility differ fundamentally in these two animal models with disturbed TG catabolism, showing a more severe phenotype by ATGL deficiency.
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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.