ArticleJVS-vascular science2022
S100A8 and S100A9 are elevated in chronically threatened ischemic limb muscle and induce ischemic mitochondrial pathology in mice.
Article in JVS-vascular science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- S100A8/S100A9 released by CD11bExperimental & molecular medicine · 2026Article
- S100A9 as a shared biomarker and mediator of metabolic dysfunction in peripheral artery disease and sarcopenia.Frontiers in genetics · 2026Article
- Multiomic Analysis of Calf Muscle in Peripheral Artery Disease and Chronic Kidney Disease.Circulation research · 2025Article
- ICAM1 blockade improves ischemic muscle reperfusion in diabetic mice.Cardiovascular diabetology · 2025Article
- A 6-Minute Limb Function Assessment for Therapeutic Testing in Experimental Peripheral Artery Disease Models.JACC. Basic to translational science · 2025Article
- Advances in the study of S100A9 in cardiovascular diseases.Cell proliferation · 2024Review
- A 6-minute Limb Function Assessment for Therapeutic Testing in Experimental Peripheral Artery Disease Models.bioRxiv : the preprint server for biology · 2024Article
- Inhibiting anti-angiogenic VEGF165b activates a miR-17-20a-Calcipressin-3 pathway that revascularizes ischemic muscle in peripheral artery disease.Communications medicine · 2024Article
- Deletion of the aryl hydrocarbon receptor in endothelial cells improves ischemic angiogenesis in chronic kidney disease.American journal of physiology. Heart and circulatory physiology · 2024Article
- Activation of the Aryl Hydrocarbon Receptor in Muscle Exacerbates Ischemic Pathology in Chronic Kidney Disease.Circulation research · 2023Article
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Authors and funding
11 authors.
Funding
Abstract
Objective: The objective of the present study was to determine whether elevated levels of S100A8 and S100A9 (S100A8/A9) alarmins contribute to ischemic limb pathology. Methods: Gastrocnemius muscle was collected from control patients without peripheral arterial disease (PAD; n = 14) and patients with chronic limb threatening limb ischemia (CLTI; n = 14). Mitochondrial function was assessed in permeabilized muscle fibers, and RNA and protein analyses were used to quantify the S100A8/A9 levels. Additionally, a mouse model of hindlimb ischemia with and without exogenous delivery of S100A8/A9 was used. Results: Compared with the non-PAD control muscles, CLTI muscles displayed significant increases in the abundance of S100A8 and S100A9 at both mRNA and protein levels ( Conclusions: The S100A8/A9 levels were increased in CLTI limb muscle specimens compared with the non-PAD control muscle specimens, and the level of accumulation was associated with muscle mitochondrial impairment. Elevated S100A8/A9 levels in mice subjected to hindlimb ischemia impaired perfusion recovery and mitochondrial function. Together, these findings suggest that the inflammatory mediators S100A8/A9 might be directly involved in ischemic limb pathology.
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