Apolipoprotein A2 Influences ANGPTL3 in Modulating TG Catabolism and Inflammatory Cytokines Secretion

Apolipoprotein A2 (ApoA2) and ANGPTL3 modulate LPL activity and inflammatory cytokine secretion, resultantly influencing TG metabolism and inflammatory response. However, any associations that exist between those modulators were not explored. The study aimed to elucidate the functions of ApoA2 in modulating ANGPTL3 on the metabolism of TG and inflammatory cytokine secretion.

A case-control hospital-based clinical study was conducted. A total of 50 patients with diagnosed CAD and 50 healthy control individuals were enrolled. Levels of ApoA2, ANGPTL3, and several pro-inflammatory cytokines were measured.

The levels of ANGPTL3 and ApoA2 exhibited no significant discordance between the CAD group and control group. Both ANGPTL3 and ApoA2 were associated with TG (r = 0.249, P = 0.002; r = 0.379, P = 0.001, respectively). Additionally, ApoA2 were inversely associated with hs-CRP (r = -0.079, P =0.003), TNF-α (r = -0.119, P = 0.001), and IL-1β (r = -0.103, P = 0.004). Regression analysis confirmed that ApoA2 was an independent modulator of TG and inflammatory cytokines independent of ANGPTL3 (standardized β = 0.196, P < 0.001).

ANGPTL3 and ApoA2 correlate with TG levels, with ApoA2 identified as an independent contributor via stepwise regression, and ANGPTL3 exerts its TGregulating effect mainly by inhibiting LPL activity through multiple mechanisms, suggesting its potential anti-inflammatory role, though conflicting findings in existing studies indicate the need for further clarification of this relationship.

ApoA2 influences ANGPTL3 in modulating catabolism of TG and atherosclerotic-related inflammatory cytokines, suggesting a vital role of ApoA2 in promoting pathological progression of CAD.