Table 1 of
Armendariz, Mol Vis 2026; 32:22-32. Table 1 of
Armendariz, Mol Vis 2026; 32:22-32.
Table 1. Indirectly modulating late stage fibrogenic potential by early targeting of the neo-microvasculature in nAMD in keeping with the concept of dynamic reciprocity.
| Target pathway | Objective/ Rationale |
|---|---|
| Permeability (beyond anti-VEGF) | Prevention of ECM ‘stretching’ and liberation of latent TGF beta Prevention of EC-induced production of abundant profibrogenic factors, downregulation of MMPs, EMT, microvascular rarefaction and premature cellular senescence. Promoting laminar flow and eNOS production Prevention of EC injury (leukocyte trafficking, recurrent leakage, coagulation) |
| Vascular maturation | Reduce permeability/neutralize hypoxia and therefore is another mechanism to target the downstream consequences of vascular permeability [58] Restoration of laminar blood flow Restoration of eNOS production Prevention of EC injury and apoptosis |
| Senescent ECs | Improved immune surveillance, elimination/reduction of SASP |
| Endothelial cell dysfunction (ECD) | Prevention of premature EC senescence Prevention of EndMT Prevention of vascular rarefaction |
| EC-associated vascular niche/ angiocrine factors | Promotion of vascular normalization in tissue repair/fibrosis |