Abstract
In peripheral arterial disease (PAD) patients, occlusions in the major arteries that supply the leg makes blood flow dependent on the capacity of neovascularization. There is no current medication that is able to increase neovascularization to the ischemic limb and directly treat the primary problem of PAD. An increasing body of evidence supports the notion that inflammation plays an important role in the vascular remodeling and perfusion recovery after PAD. Interleukins (ILs), a group of proteins produced during inflammation, have been considered to be important for angiogenesis and arteriogenesis after tissue ischemia. This review summarizes the latest clinical and experimental developments of the role of ILs in blood perfusion recovery after PAD.
Highlights
Introduction of peripheral arterial diseasePeripheral arterial disease (PAD) is caused by atherosclerosis that leads to occlusions of the arteries to the lower extremities
New capillaries grow from pre-existing vessels and form capillary networks to expand blood flow distribution in ischemic tissues downstream of the arterial occlusion, which is termed as angiogenesis [14]
While some pharmaceutical therapies with statins, and antiplatelet agents have shown some efficacy in preventing artery occlusion in PAD patients; no pharmacological agents have been able to increase neovascularization to the ischemic limb resulting from the arterial occlusions after PAD [18,19]
Summary
Introduction of peripheral arterial diseasePeripheral arterial disease (PAD) is caused by atherosclerosis that leads to occlusions of the arteries to the lower extremities. Interleukins (ILs), a group of proteins produced during inflammation, have been considered to be important for angiogenesis and arteriogenesis after tissue ischemia. In PAD patients, limb ischemia causes tissue hypoxia, which leads to the generation of hypoxia-inducible growth factors and the recruitment of inflammatory cells.
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