Review demonstrates interleukin-6 drives vascular disruption in diabetic macular edema, highlighting its potential for treatment-resistant disease.
Key Points
To review the biological role, clinical relevance, and therapeutic potential of targeting interleukin-6 in diabetic macular edema, especially in patients with incomplete responses to standard anti-VEGF therapy.
Synthesized current literature on interleukin-6 (IL-6) signaling pathways, biological functions, and elevated intraocular levels in diabetic macular edema.
Evaluated preclinical and clinical evidence regarding IL-6-targeting agents such as tocilizumab and sarilumab alone and alongside anti-VEGF therapies.
Identified IL-6 as a key hub cytokine driving chronic inflammation, blood-retinal barrier breakdown, and vascular permeability via both VEGF-dependent and VEGF-independent mechanisms.
Highlighted IL-6 inhibition as a promising therapeutic approach for patients with refractory diabetic macular edema that fails to respond adequately to standard anti-VEGF agents.