{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T18:13:20Z","timestamp":1791915200376,"version":"4.3.4"},"reference-count":133,"publisher":"MDPI AG","issue":"11","license":[{"start":{"date-parts":[[2024,10,25]],"date-time":"2024-10-25T00:00:00Z","timestamp":1729814400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National Science Center, Poland","award":["2018\/29\/B\/NZ4\/00771"],"award-info":[{"award-number":["2018\/29\/B\/NZ4\/00771"]}]},{"name":"National Science Center, Poland","award":["2019\/33\/B\/NZ4\/01760"],"award-info":[{"award-number":["2019\/33\/B\/NZ4\/01760"]}]},{"name":"National Science Center, Poland","award":["2021\/43\/B\/NZ4\/00339"],"award-info":[{"award-number":["2021\/43\/B\/NZ4\/00339"]}]},{"name":"National Science Center, Poland","award":["17GRNT32910002"],"award-info":[{"award-number":["17GRNT32910002"]}]},{"name":"American Heart Association","award":["2018\/29\/B\/NZ4\/00771"],"award-info":[{"award-number":["2018\/29\/B\/NZ4\/00771"]}]},{"name":"American Heart Association","award":["2019\/33\/B\/NZ4\/01760"],"award-info":[{"award-number":["2019\/33\/B\/NZ4\/01760"]}]},{"name":"American Heart Association","award":["2021\/43\/B\/NZ4\/00339"],"award-info":[{"award-number":["2021\/43\/B\/NZ4\/00339"]}]},{"name":"American Heart Association","award":["17GRNT32910002"],"award-info":[{"award-number":["17GRNT32910002"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Antioxidants"],"abstract":"<jats:p>The anti-oxidative and anti-inflammatory properties of high-density lipoprotein (HDL) are thought to be mediated by paraoxonase 1 (PON1), a calcium-dependent hydrolytic enzyme carried on a subfraction of HDL that also carries other anti-oxidative and anti-inflammatory proteins. In humans and mice, low PON1 activity is associated with elevated oxidized lipids and homocysteine (Hcy)-thiolactone, as well as proteins that are modified by these metabolites, which can cause oxidative stress and inflammation. PON1-dependent metabolic changes can lead to atherothrombotic cardiovascular disease, Alzheimer\u2019s disease, and cancer. The molecular bases underlying these associations are not fully understood. Biochemical, proteomic, and metabolic studies have significantly expanded our understanding of the mechanisms by which low PON1 leads to disease and high PON1 is protective. The studies discussed in this review highlight the changes in gene expression affecting proteostasis as a cause of the pro-oxidative and pro-inflammatory phenotypes associated with attenuated PON1 activity. Accumulating evidence supports the conclusion that PON1 regulates the expression of anti-oxidative and anti-inflammatory proteins, and that the disruption of these processes leads to disease.<\/jats:p>","DOI":"10.3390\/antiox13111292","type":"journal-article","created":{"date-parts":[[2024,10,25]],"date-time":"2024-10-25T03:46:04Z","timestamp":1729827964000},"page":"1292","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["The Molecular Bases of Anti-Oxidative and Anti-Inflammatory Properties of Paraoxonase 1"],"prefix":"10.3390","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5845-4409","authenticated-orcid":false,"given":"Hieronim","family":"Jakubowski","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Biotechnology, University of Life Sciences, 60-637 Pozna\u0144, Poland"},{"name":"Department of Microbiology, Biochemistry and Molecular Genetics, International Center for Public Health, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,10,25]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"868","DOI":"10.1038\/nature01323","article-title":"Inflammation in atherosclerosis","volume":"420","author":"Libby","year":"2002","journal-title":"Nature"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"1317","DOI":"10.1152\/physrev.00004.2012","article-title":"Molecular biology of atherosclerosis","volume":"93","author":"Hopkins","year":"2013","journal-title":"Physiol. 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