{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T17:04:46Z","timestamp":1778259886336,"version":"3.51.4"},"reference-count":132,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2020,9,2]],"date-time":"2020-09-02T00:00:00Z","timestamp":1599004800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Mounting evidence strongly suggests a causal link between chronic kidney disease (CKD) and cardiovascular disease (CVD). Compared with non-CKD patients, patients with CKD suffer disproportionately from CVD and derive suboptimal benefits from interventions targeting conventional CVD risk factors. Uremic toxins (UTs), whose plasma levels rapidly rise as CKD progresses, represent a unique risk factor in CKD, which has protean manifestations on CVD. Among the known UTs, tryptophan metabolites and trimethylamine N-oxide are well-established cardiovascular toxins. Their molecular mechanisms of effect warrant special consideration to draw translational value. This review surveys current knowledge on the effects of specific UTs on different pathways and cell functions that influence the integrity of cardiovascular health, with implication for CVD progression. The effect of UTs on cardiovascular health is an example of a paradigm in which a cascade of molecular and metabolic events induced by pathology in one organ in turn induces dysfunction in another organ. Deciphering the molecular mechanisms underlying such cross-organ pathologies will help uncover therapeutic targets to improve the management of CVD in patients with CKD.<\/jats:p>","DOI":"10.3390\/cells9092024","type":"journal-article","created":{"date-parts":[[2020,9,2]],"date-time":"2020-09-02T09:29:28Z","timestamp":1599038968000},"page":"2024","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Molecular Mechanisms Underlying the Cardiovascular Toxicity of Specific Uremic Solutes"],"prefix":"10.3390","volume":"9","author":[{"given":"Jonathan D.","family":"Ravid","sequence":"first","affiliation":[{"name":"Renal Section, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vipul C.","family":"Chitalia","sequence":"additional","affiliation":[{"name":"Renal Section, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA"},{"name":"Boston Veterans Affairs Healthcare System, Boston, MA 02130, USA"},{"name":"Global Cocreation Labs, Institute of Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2020,9,2]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"e016412","DOI":"10.1136\/bmjopen-2017-016412","article-title":"Prevalence, incidence and associated mortality of cardiovascular disease in patients with chronic kidney disease in low- and middle-income countries: A protocol for a systematic review and meta-analysis","volume":"7","author":"Temgoua","year":"2017","journal-title":"BMJ Open"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"559","DOI":"10.1016\/j.semnephrol.2018.08.002","article-title":"Cardiovascular Disease in Children and Adolescents with Chronic Kidney Disease","volume":"38","author":"Weaver","year":"2018","journal-title":"Semin. 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