{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T16:06:22Z","timestamp":1791389182820,"version":"4.3.3"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"14","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,7,16]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Exposure to chronic psychosocial stress is a risk factor for atherosclerosis\u2010based cardiovascular disease. We previously demonstrated the increased expressions of cathepsin S (CatS) in atherosclerotic lesions. Whether CatS participates directly in stress\u2010related neointimal hyperplasia has been unknown.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Male wild\u2010type and CatS\u2010deficient mice that underwent carotid ligation injury were subjected to chronic immobilization stress for morphological and biochemical studies at specific times. On day 14 after stress\/surgery, stress enhanced the neointima formation. At the early time points, the stressed mice had increased plaque elastin disruption, cell proliferation, macrophage accumulation,\n              <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>\n              and\/or protein levels of vascular cell adhesion molecule\u20101, angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              type 1 receptor, monocyte chemoattractant protein\u20101, gp91\n              <jats:sup>phox<\/jats:sup>\n              , stromal cell\u2013derived factor\u20101, C\u2010X\u2010C chemokine receptor\u20104, toll\u2010like receptor\u20102, toll\u2010like receptor\u20104,\n              <jats:styled-content style=\"fixed-case\">SC<\/jats:styled-content>\n              35, galectin\u20103, and CatS as well as targeted intracellular proliferating\u2010related molecules (mammalian target of rapamycin, phosphorylated protein kinase B, and p\u2010glycogen synthase kinase\u20103\u03b1\/\u03b2). Stress also increased the plaque matrix metalloproteinase\u20109 and matrix metalloproteinase\u20102\n              <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>\n              expressions and activities and aorta\u2010derived smooth muscle cell migration and proliferation. The genetic or pharmacological inhibition of CatS by its specific inhibitor (Z\u2010\n              <jats:styled-content style=\"fixed-case\">FL<\/jats:styled-content>\n              \u2010COCHO) ameliorated the stressed arterial targeted molecular and morphological changes and stressed aorta\u2010derived smooth muscle cell migration. Both the genetic and pharmacological interventions had no effect on increased blood pressure in stressed mice.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">These results demonstrate an essential role of CatS in chronic stress\u2013related neointimal hyperplasia in response to injury, possibly via the reduction of toll\u2010like receptor\u20102\/toll\u2010like receptor\u20104\u2013mediated inflammation, immune action, and smooth muscle cell proliferation, suggesting that CatS will be a novel therapeutic target for stress\u2010related atherosclerosis\u2010based cardiovascular disease.<\/jats:p>\n          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