Angiogenesis and vasculogenesis in rheumatoid arthritis

Abstract

Targeting angiogenesis and restoration of vasculogenesis may be beneficial for the therapy and outcome of RA.

Immunohistochemical evidence of stress and inflammatory markers in mouse models of cutaneous leishmaniosis

“…This treatment ameliorated the course of disease by reducing lesion size and parasite load, although no complete cure was observed [13]. VEGF is an angiogenic factor produced and secreted by a number of cell types, including muscle cells, fibroblast and macrophages [6,21,52], and induces endothelial cell proliferation and stimulates capillary formation in models of angiogenesis, such as embryonic development, wound healing, inflammatory diseases and tumors [18,21,61]. VEGF can also induce monocyte chemotaxis [19].…”

Functionalized STAT1 siRNA Nanoparticles Regress Rheumatoid Arthritis in A Mouse Model

“…As the disease progresses, these cytokines induce synoviocytes to undergo prolif eration, mix with the infiltrating immune cells, and create a new pathological tissue termed pan nus [3]. Proliferation of the synovium creates a hypoxic environment necessitating the growth of new blood vessels [4,5]. Pannus secretes enzymes that destroy cartilage and bone [6].…”

Peptide-siRNA nanocomplexes targeting NF-κB subunit p65 suppress nascent experimental arthritis

“…Although the etiology of RA remains controversial, the hallmark of the disease is characterized by inflammation of the synovial lining of diarthrodial joints, massive synovial proliferation, and an influx of inflammatory cells, macrophages, and lymphocytes through leaky angiogenic blood vessels (2)(3)(4). This cellular influx and synovial proliferation lead to the release of inflammatory cytokines and matrix-degrading enzymes, all of which contribute to the destruction of connective tissue, cartilage, and subchondral bone of the affected joints.…”