This study examined whether HepG2 hepatocyte-derived exosomes (HG-EX) worsen AMD-like retinal degeneration in A2E-laden ARPE-19 cells exposed to blue light (in vitro) and in blue-light-exposed BALB/c mice (in vivo), focusing on oxidative stress, inflammation, apoptosis, and angiogenesis.
HG-EX pretreatment significantly increased intracellular ROS and NO production, suppressed Nrf2 and SOD expression, elevated inflammasome-related and apoptosis-related proteins, and upregulated pro-angiogenic factors in ARPE-19 cells; in mice, HG-EX raised retinal COX-2, TNF-α, IL-1β, IL-6, and Bcl-2/Bax levels while reducing outer segment and inner nuclear layer thickness.
- AMD models (A2E + blue light) only approximate selected features of AMD and may not fully recapitulate human disease pathophysiology. - HepG2 is a hepatocellular carcinoma cell line; exosomes may not reflect those secreted by normal human hepatocytes. - No mechanistic pathway or specific exosomal cargo identified as the driver of retinal damage.
These findings are preclinical and not yet actionable clinically, but they raise the hypothesis that liver-derived exosomes may contribute to AMD pathogenesis via a liver-eye axis, warranting future translational investigation.
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