The iterative lipid impact on inflammation in atherosclerosis

Kraaijenhof, Jordan M; Hovingh, G. Kees; Stroes, Erik S.G.; Kroon, Jeffrey

doi:10.1097/mol.0000000000000779

Cited by 13 publications

(8 citation statements)

References 110 publications

(120 reference statements)

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“…The hypothesis that Lp(a) pathogenicity is associated with inflammation and that immune cells, and monocytes in particular, are involved, was expressed quite a long time ago [19]. The relationship between the innate immune system and Lp(a) is based on the fact that oxidized phospholipids localized on Lp(a) can be recognized by receptors of innate immunity [20].…”

Section: Discussionmentioning

confidence: 99%

Lipoprotein(a), Immune Cells and Cardiovascular Outcomes in Patients with Premature Coronary Heart Disease

Афанасьева

Tyurina

Klesareva

et al. 2022

JPM

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The detection of lipoprotein(a) [Lp(a)] in the artery wall at the stage of lipid-bands formation may indicate that it participates in the atherosclerosis local nonspecific inflammatory process. Innate immune cells are involved in atherogenesis, with monocytes playing a major role in the initiation of atherosclerosis, while neutrophils can contribute to plaque destabilization. This work studies the relationship between Lp(a), immune blood cells and major adverse cardiovascular events (MACE) in patients with the early manifestation of coronary heart disease (CHD). The study included 200 patients with chronic CHD, manifested up to the age of 55 in men and 60 in women. An increased Lp(a) concentration [hyperLp(a)] was shown to predict cardiovascular events in patients with premature CHD with long-term follow-up. According to the logistic regression analysis results, an increase in the monocyte count with OR = 4.58 (95% CI 1.04–20.06) or lymphocyte-to-monocyte ratio with OR = 0.82 (0.68–0.99), (p < 0.05 for both) was associated with MACE in patients with early CHD, regardless of gender, age, classical risk factors, atherogenic lipoproteins concentration and statin intake. The combination of an increased monocyte count and hyperLp(a) significantly increased the proportion of patients with early CHD with subsequent development of MACE (p = 0.02, ptrend = 0.003). The odds of cardiovascular events in patients with early CHD manifestation were highest in patients with an elevated lymphocyte-to-monocyte ratio and an elevated Lp(a) level. A higher neutrophil blood count and an elevated neutrophil-to-lymphocyte ratio determined the faster development of MACE in patients with a high Lp(a) concentration. The data obtained in this study suggest that the high atherothrombogenicity of Lp(a) is associated with the “inflammatory” component and the innate immune cells involvement in this process. Thus, the easily calculated immunological ratios of blood cells and Lp(a) concentrations can be considered simple predictors of future cardiovascular events.

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Section: Discussionmentioning

confidence: 99%

Lipoprotein(a), Immune Cells and Cardiovascular Outcomes in Patients with Premature Coronary Heart Disease

Афанасьева

Tyurina

Klesareva

et al. 2022

JPM

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“…However, modified lipids within these particles act as bioactive molecules conferring other biological activities not shown in unmodified LDLs [ 100 , 101 ]. These bioactive lipids might induce a pro-inflammatory response in ECs and macrophages [ 102 , 103 , 104 ]. On the other hand, when LDLs are extensively modified, they become unrecognizable by the LDLR, while allowing recognition by a range of scavenger receptors [ 105 , 106 , 107 , 108 ].…”

Section: Atherosclerosis Initiation and Fatty Streak Formationmentioning

confidence: 99%

Pathophysiology of Atherosclerosis

Jebari-Benslaiman

Galicia-García

Larrea-Sebal

et al. 2022

IJMS

251

191

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Atherosclerosis is the main risk factor for cardiovascular disease (CVD), which is the leading cause of mortality worldwide. Atherosclerosis is initiated by endothelium activation and, followed by a cascade of events (accumulation of lipids, fibrous elements, and calcification), triggers the vessel narrowing and activation of inflammatory pathways. The resultant atheroma plaque, along with these processes, results in cardiovascular complications. This review focuses on the different stages of atherosclerosis development, ranging from endothelial dysfunction to plaque rupture. In addition, the post-transcriptional regulation and modulation of atheroma plaque by microRNAs and lncRNAs, the role of microbiota, and the importance of sex as a crucial risk factor in atherosclerosis are covered here in order to provide a global view of the disease.

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“…This could in part be explained by the longer plasma residence time of Lp(a), which results in a more oxidized state. 28 In addition, previous reports suggest that the apo(a) component of Lp(a) is highly homologous to plasminogen, being able to inhibit activation of plasminogen to plasmin by endogenous tissue plasminogen activators as well as competing for binding of plasminogen and plasmin to established fibrin clots, showing a clear antifibrinolytic effect. 29 This dual pathophysiological mechanism, promoter of atherosclerosis and simultaneous generator of a pro-thrombotic state, is very similar to what occurs in CLI.…”

Section: Discussionmentioning

confidence: 99%

Elevated lipoprotein (a) levels and risk of peripheral artery disease outcomes: A systematic review

Masson

Lobo²,

Barbagelata

et al. 2022

Vasc Med

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Background: Despite strong association of elevated lipoprotein (a) (Lp(a)) levels with incident coronary and cerebrovascular disease, data for incident peripheral artery disease (PAD) are less robust. The main objective of the present systematic review was to analyze the association between elevated Lp(a) levels and PAD outcomes. Methods: This systematic review was performed according to PRISMA guidelines. A literature search was performed to detect randomized clinical trials or observational studies with a cohort design that evaluated the association between Lp(a) levels and PAD outcomes. Results: Fifteen studies including 493,650 subjects were identified and considered eligible for this systematic review. This systematic review showed that the vast majority of the studies reported a significant association between elevated Lp(a) levels and the risk of PAD outcomes. The elevated Lp(a) levels were associated with a higher risk of incident claudication (RR: 1.20), PAD progression (HR: 1.41), restenosis (HR: 6.10), death and hospitalization related to PAD (HR: 1.37), limb amputation (HR: 22.75), and lower limb revascularization (HR: 1.29 and 2.90). In addition, the presence of elevated Lp(a) values were associated with a higher risk of combined PAD outcomes, with HRs in a range between 1.14 and 2.80, despite adjusting for traditional risk factors. Heterogeneity of results can be explained by different patient populations studied and varying Lp(a) cut-off points of Lp(a) analyzed. Conclusion: This systematic review suggests that evidence is available to support an independent positive association between Lp(a) levels and the risk of future PAD outcomes. PROSPERO Registration No.: 289253.

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The iterative lipid impact on inflammation in atherosclerosis

Cited by 13 publications

References 110 publications

Lipoprotein(a), Immune Cells and Cardiovascular Outcomes in Patients with Premature Coronary Heart Disease

Lipoprotein(a), Immune Cells and Cardiovascular Outcomes in Patients with Premature Coronary Heart Disease

Pathophysiology of Atherosclerosis

Elevated lipoprotein (a) levels and risk of peripheral artery disease outcomes: A systematic review

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