{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T23:09:25Z","timestamp":1777936165850,"version":"3.51.4"},"reference-count":22,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2022,10,6]],"date-time":"2022-10-06T00:00:00Z","timestamp":1665014400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Inner Mongolia Autonomous Region Higher Education Scientific Research Funding Project","award":["No. NJZY21051"],"award-info":[{"award-number":["No. NJZY21051"]}]},{"name":"Funded by Tianjin Key Medical Discipline(Specialty) Construction Project"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Vasc Access"],"published-print":{"date-parts":[[2024,3]]},"abstract":"<jats:sec>\n                    <jats:title>Purpose:<\/jats:title>\n                    <jats:p>This study aimed to determine the effect of pentoxifylline (PTX) on the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome pathway and its role in preventing arteriovenous fistula (AVF) failure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Vein samples were collected from AVF failure patients and from patients who underwent surgical AVF as a control. The expressions of CD34 and NLRP3 in AVF tissues were detected by immunohistochemistry and Western blotting. Arteriovenous fistula rat models were established by the end-to-end anastomosis of the common carotid artery and external jugular vein. The AVF models were divided into the following groups: AVF, AVF\u2009+\u2009PTX, AVF\u2009+\u2009uraemia and AVF\u2009+\u2009uraemia\u2009+\u2009PTX. Six weeks after surgery, the AVF tissues in each group were collected to detect the expressions of CD34, NLRP3, caspase-1 and interleukin (IL)-1\u03b2 by immunohistochemistry, Western blotting and real-time polymerase chain reaction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>The expressions of NLRP3 and CD34 in human AVF failure tissues were significantly higher than those in normal veins ( p\u2009&lt;\u20090.001), indicating that NLRP3 was upregulated in patients with AVF failure. In our animal study, the veins in the AVF\u2009+\u2009uraemia group exhibited heavy hyperplasia, and the boundary between the media and the adventitia was not clear. However, PTX alleviated this hyperplasia. Compared with the AVF models, the AVF\u2009+\u2009uraemia models had much higher expressions of NLRP3, caspase-1, IL-1\u03b2 and CD34 ( p\u2009&lt;\u20090.001). However, PTX had the opposite effect against uraemia on the NLRP3 inflammasome pathway at both the gene and protein levels.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Our findings provide new insights that show that PTX can decrease the activity of the NLRP3 inflammasome pathway in AVF models. Pentoxifylline has the potential as a drug for preventing intimal hyperplasia and AVF failure.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/11297298221124730","type":"journal-article","created":{"date-parts":[[2022,10,7]],"date-time":"2022-10-07T01:38:45Z","timestamp":1665106725000},"page":"566-575","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["Pentoxifylline decreases the activity of the nucleotide-binding oligomerization domain-like receptor protein 3 pathway: potential role for preventing arteriovenous fistula stenosis"],"prefix":"10.1177","volume":"25","author":[{"given":"Tao","family":"Feng","sequence":"first","affiliation":[{"name":"NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, 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