[1] A study published in 2019 found that AIM exhibited a broader expression pattern in dogs than previously observed in humans and mice.
The study on mature healthy Beagles revealed AIM expression in tissue macrophages of the spleen, liver, lungs, lymph nodes, and proximal tubules in the kidney.
Its diverse functions include regulating intracellular processes such as lipid metabolism and apoptosis, inhibiting cholesterol synthesis, and influencing Th17 cell pathogenicity.
The specific receptor for AIM is unclear, but it can bind to molecules like CD36, a membrane glycoprotein involved in various cellular functions, including inflammation and atherosclerosis.
This response is crucial for recruiting adipose tissue macrophages, facilitated by AIM-induced chemokine production through toll-like receptor 4 (TLR4) activation.
Administering recombinant AIM to TLR4-deficient mice induces lipolysis without chemokine production, preventing inflammatory macrophage infiltration into adipose tissue and mitigating obesity-related inflammation, insulin resistance, and glucose intolerance.
In ALS, secondary progressive multiple sclerosis, rheumatoid arthritis, and osteoarthritis, AIM levels are elevated, making it a sensitive biomarker for disease activity.
[1] The role of AIM in cardiovascular and pulmonary diseases centers around inflammation, inhibiting macrophage apoptosis, and enhancing inflammatory responses.
AIM deficiency in mice shows improved outcomes after myocardial infarction, including increased survival, reduced heart rupture, and altered macrophage profiles.
[1] In serum, AIM, released from the IgM pentamer, serves diverse purposes, including its involvement in acute kidney injury (AKI) .
A 2016 study published in Nature Medicine highlighted the role of apoptosis inhibitor of macrophage in promoting recovery from AKI in mice.