AI Article Synopsis
- Acute limb ischemia (ALI) occurs when blood flow to a limb is suddenly reduced, leading to a lack of oxygen and nutrients in the tissues, which can cause severe complications even after treatment.
- The text reviews various molecular and cellular factors involved in ALI, focusing on arterial thrombosis, embolism, and the subsequent ischemia/reperfusion (I/R) syndrome that can occur after restoring blood flow.
- It highlights the significance of inflammation, apoptosis, and other tissue damage mechanisms in ALI, while also discussing potential novel biomarkers and targeted therapies for better management.
Article Abstract
Acute limb ischemia (ALI) is defined as a sudden reduction in blood flow to a limb, resulting in cessation of blood flow and, therefore, cessation of the delivery of nutrients and oxygen to the tissues of the lower limb. Despite optimal treatment to restore blood flow to ischemic tissues, some patients may suffer from ischemia/reperfusion (I/R) syndrome, the most severe complication after a revascularization procedure used to restore blood flow. There are multiple molecular and cellular factors that are involved in each phase of ALI. This review focuses firstly on molecular and cellular factors of arterial thrombosis, highlighting the role of atherosclerotic plaques, smooth muscle cells (SMCs), and cytokine which may alter key components of the extracellular matrix (ECM). Then, molecular and cellular factors of arterial embolism will be discussed, highlighting the importance of thrombi composition. Molecular and cellular factors of ischemia/reperfusion syndrome are analyzed in depth, highlighting several important mechanisms related to tissue damage, such as inflammation, apoptosis, autophagy, necrosis, and necroptosis. Furthermore, local and general complications of ALI are discussed in the context of molecular alterations. Ultimately, the role of novel biomarkers and targeted therapies is discussed.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11274792 | PMC |
| http://dx.doi.org/10.3390/biom14070838 | DOI Listing |
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