Study summary · research use only
Cathelicidin LL-37-ApoB-100 interaction promotes LDL clearance and attenuates cholesterol accumulation in the liver
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study examined how the human cathelicidin peptide LL-37 interacts with LDL cholesterol, using hepatocytes, macrophages, and Apoe-/- mice with hypercholesterolemia. LL-37 was found to bind LDL via apolipoprotein B-100 domains, increasing ApoB-100 solubility and inhibiting LDL modification and aggregation. This interaction was associated with increased LDL uptake through the LDL receptor in hepatocytes and macrophages, and with increased LDL cholesterol clearance via cholesterol excretion and efflux. In Apoe-/- mice, the murine homolog cathelicidin Cramp similarly accelerated cholesterol clearance and reduced hepatic lipid accumulation. The authors describe LL-37 as an endogenous regulator of LDL that promotes its cholesterol clearance.
Abstract
Dysregulation of low-density lipoprotein (LDL) cholesterol is strongly correlated with the risk of metabolic dysfunction-associated steatotic liver disease. Endogenous molecules targeting LDL clearance play crucial roles in the progression of liver steatosis. Human cathelicidin LL-37 can form complexes with lipoproteins, but whether these complexes regulate lipoprotein-driven cholesterol metabolism is not clear. Here, we find that cathelicidin LL-37 binds to LDL via apolipoprotein (Apo)B-100 domains, enhancing the solubility of ApoB-100 and inhibiting the modifications and aggregation of LDL. LL-37-LDL interaction promotes LDL uptake through LDL receptor (LDLR) both in hepatocytes and macrophages. This interaction also promotes LDL cholesterol clearance by facilitating cholesterol excretion and cholesterol efflux. In Apoe-/- mice with hypercholesterolemia, the murine homolog cathelicidin Cramp similarly accelerates cholesterol clearance by activating cholesterol excretion and preventing hepatic lipid accumulation. This study identifies LL-37 as an endogenous regulator of LDL that promotes LDL cholesterol clearance.
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