{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T02:40:48Z","timestamp":1787452848077,"version":"build-2736575974"},"reference-count":36,"publisher":"Frontiers Media SA","issue":"9","license":[{"start":{"date-parts":[[2015,1,13]],"date-time":"2015-01-13T00:00:00Z","timestamp":1421107200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Exp Biol Med (Maywood)"],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:p>\n                    Our recent studies indicate that the transient receptor potential vanilloid type 1 (TRPV1) channel may act as a potential regulator of monocyte\/macrophage recruitment to reduce renal injury in salt-sensitive hypertension. This study tests the hypothesis that deletion of TRPV1 exaggerates salt-sensitive hypertension-induced renal injury due to enhanced inflammatory responses via monocyte chemoattractant protein-1 (MCP-1)\/C-C chemokine receptor 2 (CCR2)-dependent pathways. Wild type (WT) and TRPV1-null mutant (TRPV1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) mice were subjected to uninephrectomy and deoxycorticosterone acetate (DOCA)-salt treatment for four weeks with or without the selective CCR2 antagonist, RS504393. DOCA-salt treatment increased systolic blood pressure (SBP) to the same degree in both strains, but increased urinary excretion of albumin and 8-isoprostane and decreased creatinine clearance with greater magnitude in TRPV1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice compared to WT mice. DOCA-salt treatment also caused renal glomerulosclerosis, tubulointerstitial injury, collagen deposition, monocyte\/macrophage infiltration, proinflammatory cytokine and chemokine production, and NF-\u03baB activation in greater degree in TRPV1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice compared to WT mice. Blockade of the CCR2 with RS504393 (4\u2009mg\/kg\/day) had no effect on SBP in DOCA-salt-treated WT or TRPV1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice compared to their respective controls. However, treatment with RS504393 ameliorated renal dysfunction and morphological damage, and prevented the increase in monocyte\/macrophage infiltration, cytokine\/chemokine production, and NF-\u03baB activity in both DOCA-salt hypertensive strains with a greater effect in DOCA-salt-treated TRPV1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice compared to DOCA-salt-treated WT mice. No differences in CCR2 protein expression in kidney were found between DOCA-salt-treated WT and TRPV1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice with or without RS504393 treatment. Our studies for the first time indicate that deletion of TRPV1 aggravated renal injury in salt-sensitive hypertension via enhancing MCP-1\/CCR2 signaling-dependent inflammatory responses.\n                  <\/jats:p>","DOI":"10.1177\/1535370214565970","type":"journal-article","created":{"date-parts":[[2015,1,14]],"date-time":"2015-01-14T00:57:04Z","timestamp":1421197024000},"page":"1223-1234","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":20,"title":["Role of the monocyte chemoattractant protein-1\/C-C chemokine receptor 2 signaling pathway in transient receptor potential vanilloid type 1 ablation-induced renal injury in salt-sensitive hypertension"],"prefix":"10.3389","volume":"240","author":[{"given":"Youping","family":"Wang","sequence":"first","affiliation":[{"name":"Central Laboratory and Division of Cardiology, First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou 450000, 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