Skip to main content
. Author manuscript; available in PMC: 2023 Jul 21.
Published in final edited form as: Cardiol Cardiovasc Med. 2023 Apr 20;7(2):129–140. doi: 10.26502/fccm.92920318

Figure 2:

Figure 2:

Schematics of possible targets in OSM-HIF1α-PAI-1 axis to enhance vascular remodeling and AVF maturation. Targeting circulating OSM in chronic inflammation may attenuate downstream signaling cascade and may enhance favorable vascular remodeling. Among downstream signals, targeting STAT3, oxidative stress, and PAI-1 may modulate cascade toward favorable ECM and vascular remodeling via inhibition of plasmin formation and overexpression of MMPs. Oncostatin-M (OSM), Oncostatin M receptor (OSMR), Janus kinase (JAK)/signal transducer and activator of transcription (STAT), hypoxia-inducible factor-1-alpha (HIF-1α), extra cellular matrix (ECM), vascular smooth muscle cells (VSMCs), matrix metalloproteinases (MMPs).