Ask about this productRelated genes to: CETP Blocking Peptide
- Gene:
- CETP NIH gene
- Name:
- cholesteryl ester transfer protein
- Previous symbol:
- -
- Synonyms:
- BPIFF
- Chromosome:
- 16q13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-17
Related products to: CETP Blocking Peptide
Related articles to: CETP Blocking Peptide
- Increasing evidence has implicated lipoprotein (a) (Lp(a)) in the causality of cardiovascular disease. While measuring Lp(a) has an established role in cardiovascular risk assessment and triaging patients for more intensive risk factor control, there is considerable interest in the ability of medical therapies to lower Lp(a) levels. While statins have been reported to increase Lp(a) levels, a number of existing lipid-lowering interventions have been reported to modestly lower Lp(a) levels, with evidence that this contributes to the reduction in cardiovascular risk observed with proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors. Lp(a) lowering has also been reported with emerging therapies via direct inhibition of apolipoprotein A (Apo A) synthesis or Lp(a) particle formation and indirectly in response to treatment with cholesteryl ester transfer protein (CETP) inhibitors. This article will review the effects of these therapies and implications for cardiovascular risk. - Source: PubMed
Publication date: 2026/04/28
Nicholls Stephen JNelson Adam J - : Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality among individuals with type 2 diabetes mellitus (T2DM). Although women generally exhibit a more favorable cardiovascular risk profile than men in the general population, this protection is substantially reduced in the presence of diabetes, resulting in a disproportionately greater relative increase in CVD risk among women. : This review aims to integrate the roles of metabolic phenotypes, dietary exposures, and genetic susceptibility in shaping cardiovascular risk in women with T2DM, with a focus on diet-gene and diet-epigenetic interactions across critical stages of the female life course. : A narrative review of epidemiological, clinical, and mechanistic evidence from recent literature was conducted to synthesize current knowledge on sex-specific cardiometabolic pathways and nutritional determinants of vascular risk in T2DM. : Current evidence indicates that several interconnected mechanisms contribute to enhanced cardiovascular vulnerability in diabetic women, including (i) adipose tissue dysfunction and ectopic fat accumulation; (ii) insulin resistance with metabolic inflexibility and lipotoxicity; and (iii) endothelial and microvascular dysfunction driven by impaired nitric oxide signaling. Dietary patterns modulate these pathways through effects on inflammation, oxidative stress, postprandial lipid metabolism, and vascular function. Emerging evidence highlights that genetic variants (e.g., APOE; CETP; TCF7L2) significantly modify metabolic responses to dietary exposures in patients with T2DM; supporting a role for nutrigenetic interactions in shaping cardiovascular risk. In parallel, diet-related epigenetic mechanisms-including metabolic memory and early-life programming-may contribute to long-term and potentially intergenerational cardiometabolic risk. : Integrating dietary patterns with genetic susceptibility and epigenetic regulation provides a mechanistic framework for understanding the disproportionate cardiovascular risk in diabetic women and supports the development of sex-specific, life-course-oriented precision nutrition strategies for cardiovascular risk reduction. - Source: PubMed
Publication date: 2026/04/12
Ábel TatjanaGellért DiánaCsobod Csajbókné ÉvaMák Erzsébet - Different classes of chemical compounds including persistent, mobile chemicals (PMCs) often bypass the conventional treatment processes of common effluent treatment plants (CETPs), resulting in their unmonitored release into aquatic environments. In this study, an integrated treatment system comprising a microaerophilic fixed-film bioreactor (MFB) and an aerobic membrane bioreactor (Ae-MBR) was engineered to treat secondary CETP effluent. Two types of packing materials in the engineered MFBs were evaluated: one with wood charcoal (C-MFB) and another with 30% (w/w) biochar-augmented charcoal (BAC-MFB). The BAC-MFB showed better treatment efficiency, achieving 69.17% colour (Pt-Co units) removal and 93.01% COD removal at an optimal 3d hydraulic retention time (HRT). Integration with Ae-MBR further enhanced the treatment, achieving > 95% COD and > 94% colour removal, with an overall > 85% reduction in total number of parent chemical compounds and a specific > 83% reduction in PMCs from CETP effluent. At 3d HRT, bacterial community analysis revealed dominance of Campylobacterota and Bacillota in BAC-MFB under microaerophilic conditions, whereas Bacillota dominated in the Ae-MBR under aerobic conditions. The predicted metagenome analysis revealed significant enrichment of benzoate and aminobenzoate degradation pathways in the integrated system. While the BAC-MFB treatment alone achieved sufficient COD removal, its integration with Ae-MBR markedly enhanced the reduction in overall chemical complexity including PMCs from the CETP effluent. This study demonstrates that the engineered hybrid BAC-MFB-Ae-MBR system is a sustainable solution for the treatment of industrial CETP effluents. - Source: PubMed
Publication date: 2026/04/30
Thakkar ShaliniRathour RohitRana Soujanya ShekharSamant ShwetaKikani Bhavtosh AMadamwar DattaDesai Chirayu - - Source: PubMed
Publication date: 2026/04/29
Pirillo AngelaCatapano Alberico L - High-density lipoprotein cholesterol (HDL-C) is traditionally viewed as cardioprotective; however, some patients with coronary artery disease (CAD) may present with elevated HDL-C levels, challenging this assumption. This study aimed to investigate the roles of HDL subclasses, apolipoproteins, and cholesteryl ester transfer protein (CETP) activity and mass in patients with CAD with high HDL-C and low-density lipoprotein cholesterol (LDL-C) levels. - Source: PubMed
Publication date: 2026/04/27
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