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. 2022 Jan 5;36(2):328–340. doi: 10.1038/s41433-021-01807-4

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© The Author(s) 2021, corrected publication 2022

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Fig. 2 — Increased levels of LRG1 are often reported in disease and several pathogenic mechanisms involving LRG1 have been proposed. LRG1 can play a part in the immune response by modulating lymphocyte number, granulopoiesis and neutrophil function and possibly by regulating TGFβ-mediated EC-leukocyte interactions. Many cell types like fibroblasts, epithelial cells, endothelial cells and pericytes can undergo trans-differentiation to myofibroblasts and contribute to fibrosis, and LRG1 has been implicated in the conversion of fibroblasts into fibrogenic myofibroblasts in a model of lung fibrosis. Leukostasis is a feature of DR in which neutrophils adhere to the non-perfused capillaries; LRG1 might be released by adherent neutrophils and mediate the EC damage which is associated with leukostasis. LRG1 upregulation during pathological angiogenesis is required for the TGFβ-induced angiogenic switch of ECs. Vascular instability/dysfunction follows altered physical and chemical interactions between ECs and pericytes; the TGFβ family of ligands and receptors plays an essential role in vessel maturation and homoeostasis by regulating these interactions, LRG1 has been shown to impact TGFβ signalling on both ECs and pericytes. Created with BioRender.com.