ArticleProceedings of the National Academy of Sciences of the United States of America2011
Apoptosis inhibitor of macrophage (AIM) is required for obesity-associated recruitment of inflammatory macrophages into adipose tissue.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 89 citations in OpenAlex.
- Tandem mass tag-based serum proteomic profiling revealed diabetic foot ulcer pathogenesis and potential therapeutic targets.Bioengineered · 2022Trial
- The Involvement of Apoptosis Inhibitor of Macrophage in the Disease Severity of Primary Biliary Cholangitis.Journal of clinical medicine · 2026Article
- Rejuvenation of white adipose tissue in a longitudinal heterochronic transplantation model.bioRxiv : the preprint server for biology · 2025Article
- Acid ceramidase as a novel target for adiponectin receptor agonist to abrogate podocyte NLRP3 inflammasome activation and glomerular inflammation during obesity.The Journal of pharmacology and experimental therapeutics · 2025Article
- Apoptosis Inhibitor of Macrophage (AIM) Modulates Calcium Oxalate-Induced Ureteral Fibrosis in AIM-Felinized Mice.International journal of molecular sciences · 2025Article
- Endogenous CD5L controls the metabolic and inflammatory state of human macrophages.Frontiers in immunology · 2025Article
- Administration of an antibody against apoptosis inhibitor of macrophage prevents aortic aneurysm progression in mice.Scientific reports · 2024Article
- The effects of apoptosis inhibitor of macrophage in kidney diseases.European journal of medical research · 2024Review
- Macrophage lineage cells-derived migrasomes activate complement-dependent blood-brain barrier damage in cerebral amyloid angiopathy mouse model.Nature communications · 2023Article
- IgA nephropathy associated with Crohn's disease.World journal of methodology · 2023Review
- The comprehensive role of apoptosis inhibitor of macrophage (AIM) in pathological conditions.Clinical and experimental immunology · 2023Review
- The Presence of Psoriasis, Metabolic Syndrome and Their Combination Increases the Serum Levels of CRP and CD5L but Not sCD200R1 and sTLR2 in Participants.Journal of personalized medicine · 2022Article
- Article
- Multifaceted Roles of CD5L in Infectious and Sterile Inflammation.International journal of molecular sciences · 2021Review
- Role of Kallikrein 7 in Body Weight and Fat Mass Regulation.Biomedicines · 2021Article
- Apoptosis inhibitor of macrophage (AIM) contributes to IL-10-induced anti-inflammatory response through inhibition of inflammasome activation.Cell death & disease · 2021Article
- Increase in CD5L expression in the synovial membrane of knee osteoarthritis patients with obesity.Central-European journal of immunology · 2021Article
- Association between apoptosis inhibitor of macrophage and microsatellite instability status in colorectal cancer.BMC gastroenterology · 2020Article
- Role of the Scavenger Receptor CD36 in Accelerated Diabetic Atherosclerosis.International journal of molecular sciences · 2020Article
- Crucial Role of AIM/CD5L in the Development of Glomerular Inflammation in IgA Nephropathy.Journal of the American Society of Nephrology : JASN · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infiltration of inflammatory macrophages into adipose tissues with the progression of obesity triggers insulin resistance and obesity-related metabolic diseases. We recently reported that macrophage-derived apoptosis inhibitor of macrophage (AIM) protein is increased in blood in line with obesity progression and is incorporated into adipocytes, thereby inducing lipolysis in adipose tissue. Here we show that such a response is required for the recruitment of adipose tissue macrophages. In vitro, AIM-dependent lipolysis induced an efflux of palmitic and stearic acids from 3T3-L1 adipocytes, thereby stimulating chemokine production in adipocytes via activation of toll-like receptor 4 (TLR4). In vivo administration of recombinant AIM to TLR4-deficient (TLR4(-/-)) mice resulted in induction of lipolysis without chemokine production in adipose tissues. Consistently, mRNA levels for the chemokines that affect macrophages were far lower in AIM-deficient (AIM(-/-)) than in wild-type (AIM(+/+)) obese adipose tissue. This reduction in chemokine production resulted in a marked prevention of inflammatory macrophage infiltration into adipose tissue in obese AIM(-/-) mice, although these mice showed more advanced obesity than AIM(+/+) mice on a high-fat diet. Diminished macrophage infiltration resulted in decreased inflammation locally and systemically in obese AIM(-/-) mice, thereby protecting them from insulin resistance and glucose intolerance. These results indicate that the increase in blood AIM is a critical event for the initiation of macrophage recruitment into adipose tissue, which is followed by insulin resistance. Thus, AIM suppression might be therapeutically applicable for the prevention of obesity-related metabolic disorders.
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