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Title:
Caspase-1 Plays a Critical Role in Accelerating Chronic Kidney Disease-Promoted Neointimal Hyperplasia in the Carotid Artery | Journal of Cardiovascular Translational Research
Description:
To determine whether caspase-1 is critical in chronic kidney disease (CKD)-mediated arterial neointimal hyperplasia (NH), we utilized caspaseā/ā mice and induced NH in carotid artery in a CKD environment, and uremic sera-stimulated human vascular smooth muscle cells (VSMC). We made the following findings: (1) Caspase-1 inhibition corrected uremic sera-mediated downregulation of VSMC contractile markers, (2) CKD-promoted NH was attenuated in caspaseā/ā mice, (3) CKD-mediated downregulation of contractile markers was rescued in caspase null mice, and (4) expression of VSMC migration molecule αvβ3 integrin was reduced in caspaseā/ā tissues. Our results suggested that caspase-1 pathway senses CKD metabolic danger signals. Further, CKD-mediated increase of contractile markers in VSMC and increased expression of VSMC migration molecule αvβ3 integrin in NH formation were caspase-1 dependent. Therefore, caspase-1 is a novel therapeutic target for the suppression of CKD-promoted NH.
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article, pubmed, research, google, scholar, support, cas, kidney, disease, vascular, govt, journal, caspase, chronic, nonus, central, cardiovascular, neointimal, access, review, nih, extramural, hyperplasia, smooth, muscle, mice, american, ferrer, monroy, vsmc, cell, choi, ckd, medicine, nephrology, lee, privacy, cookies, content, critical, artery, lopezpastrana, wang, cells, atherosclerosis, yin, university, temple, information, publish,
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end-stage renal disease month download article/chapter nlrp3/asc inflammasome-mediated activation xiao-feng yangĀ &Ā eric chronic kidney disease chronic renal failure p-selectin-deficient mice xiao-feng yang ckd-mediated downregulation full article pdf guideline practice guideline american heart association venous neointimal hyperplasia related subjects metabolic disease research caspase-1-sirtuin 1 pathway ya-feng li ckd-mediated increase privacy choices/manage cookies ckd-promoted nh bone marrow apoptosis kidney diseases pulmonary vascular remodeling inflammasome adaptor molecule kidney disease dialysis access stenosis jahaira lopez-pastrana utilized caspaseā/ā mice caspase null mice cardiovascular translational research vascular access cardiovascular phenotype european economic area altered cytokine export superoxide dismutase mimetic lewis katz school north broad street biophysical research communications conditions privacy policy ckd accelerates development nature reviews cancer ethics declarations funding editorial research support article log cardiovascular mortality accepting optional cookies sudden coronary death extramural research support cell increases cardiovascular disease
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headline:Caspase-1 Plays a Critical Role in Accelerating Chronic Kidney Disease-Promoted Neointimal Hyperplasia in the Carotid Artery
description:To determine whether caspase-1 is critical in chronic kidney disease (CKD)-mediated arterial neointimal hyperplasia (NH), we utilized caspaseā/ā mice and induced NH in carotid artery in a CKD environment, and uremic sera-stimulated human vascular smooth muscle cells (VSMC). We made the following findings: (1) Caspase-1 inhibition corrected uremic sera-mediated downregulation of VSMC contractile markers, (2) CKD-promoted NH was attenuated in caspaseā/ā mice, (3) CKD-mediated downregulation of contractile markers was rescued in caspase null mice, and (4) expression of VSMC migration molecule αvβ3 integrin was reduced in caspaseā/ā tissues. Our results suggested that caspase-1 pathway senses CKD metabolic danger signals. Further, CKD-mediated increase of contractile markers in VSMC and increased expression of VSMC migration molecule αvβ3 integrin in NH formation were caspase-1 dependent. Therefore, caspase-1 is a novel therapeutic target for the suppression of CKD-promoted NH.
datePublished:2016-02-29T00:00:00Z
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Vascular inflammation
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description:To determine whether caspase-1 is critical in chronic kidney disease (CKD)-mediated arterial neointimal hyperplasia (NH), we utilized caspaseā/ā mice and induced NH in carotid artery in a CKD environment, and uremic sera-stimulated human vascular smooth muscle cells (VSMC). We made the following findings: (1) Caspase-1 inhibition corrected uremic sera-mediated downregulation of VSMC contractile markers, (2) CKD-promoted NH was attenuated in caspaseā/ā mice, (3) CKD-mediated downregulation of contractile markers was rescued in caspase null mice, and (4) expression of VSMC migration molecule αvβ3 integrin was reduced in caspaseā/ā tissues. Our results suggested that caspase-1 pathway senses CKD metabolic danger signals. Further, CKD-mediated increase of contractile markers in VSMC and increased expression of VSMC migration molecule αvβ3 integrin in NH formation were caspase-1 dependent. Therefore, caspase-1 is a novel therapeutic target for the suppression of CKD-promoted NH.
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