ArticleCell death discovery2024
CCL11 released by GSDMD-mediated macrophage pyroptosis regulates angiogenesis after hindlimb ischemia.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- The CCL11-CCR3 Axis Regulates the Aggravation of Neuroinflammation in Astrocytic Necroptosis After Cerebral Ischemia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Phillyrin promotes flap survival by mitigating pyroptosis through the TLR4/NF-κB/NLRP3 signaling pathway.Apoptosis : an international journal on programmed cell death · 2026Article
- Targeting gasdermin D-mediated pyroptosis: a precision anti-inflammatory strategy for acute and chronic lung diseases.Inflammopharmacology · 2026Review
- Mendelian randomization analysis of druggable gene expression in liver cancer risk and autoimmune hepatitis.Discover oncology · 2025Article
- Exercise sensitizes the pressure diuresis response: shifting immune landscapes may underlie renal adaptations.American journal of physiology. Renal physiology · 2025Article
- Changes and Diagnostic Value of Serum CCL26 and CCR3 in T2DM with Lower Extremity Artery Disease.Vascular health and risk management · 2025Article
- Licochalcone A suppresses pancreatic ductal adenocarcinoma progression by targeting eEF2K-mediated pyroptosis.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral vascular disease (PVD) is an emerging public health burden with a high rate of disability and mortality. Gasdermin D (GSDMD) has been reported to exert pyroptosis and play a critical role in the pathophysiology of many cardiovascular diseases. We ought to determine the role of GSDMD in the regulation of perfusion recovery after hindlimb ischemia (HLI). Our study revealed that GSDMD-mediated pyroptosis occurred in HLI. GSDMD deletion aggravated perfusion recovery and angiogenesis in vitro and in vivo. However, how GSDMD regulates angiogenesis after ischemic injury remains unclear. We then found that GSDMD-mediated pyroptosis exerted the angiogenic capacity in macrophages rather than endothelial cells after HLI. GSDMD deletion led to a lower level of CCL11 in mice serum. GSDMD knockdown in macrophages downregulated the expression and decreased the releasing level of CCL11. Furthermore, recombinant CCL11 improved endothelial functions and angiogenesis, which was attenuated by CCL11 antibody. Taken together, these results demonstrate that GSDMD promotes angiogenesis by releasing CCL11, thereby improving blood flow perfusion recovery after hindlimb ischemic injury. Therefore, CCL11 may be a novel target for prevention and treatment of vascular ischemic diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.