Inhibiting MiR-33a-3p Expression Fails to Enhance ApoAI-Mediated Cholesterol Efflux in Pro-Inflammatory Endothelial Cells DOI Creative Commons
Kun Huang,

Achala Pokhrel,

Jing Echesabal-Chen

et al.

Medicina, Journal Year: 2025, Volume and Issue: 61(2), P. 329 - 329

Published: Feb. 13, 2025

Background and Objectives: Atherosclerosis is an inflammatory condition that results in cholesterol accumulating within vessel wall cells. Atherosclerotic cardiovascular disease the leading cause of mortality worldwide due to this being a major contributor myocardial infarctions cerebrovascular accidents. Research suggests accumulation occurring precisely arterial endothelial cells triggers atherogenesis exacerbates atherosclerosis. Furthermore, inflamed endothelium acts as catalyst for atherosclerotic development. Therefore, enhancing removal specifically pro-inflammatory may be potential treatment option While we have previously shown inhibiting microRNA guide strand miR-33a-5p increases both ABCA1 expression apoAI-mediated efflux, it unknown whether miR-33a-3p passenger causes similar atheroprotective effects. In study, what aimed test. Materials Methods: We used plasmid transfection knockdown cultured immortalized mouse aortic (iMAECs). compared efflux these iMAECs transfected with control plasmid. Results: The resulted significant increase mRNA expression. However, inhibition did not significantly protein iMAECs. Moreover, failed detect from knockdown. Conclusions: Our indicative alone does enhance ABCA1-dependent To gain any benefit endothelium, additional anti-atherogenic strategies would likely needed unison.

Language: Английский

Role of CETP, PCSK-9, and CYP7-alpha in cholesterol metabolism: Potential targets for natural products in managing hypercholesterolemia DOI Creative Commons
Rita Ngozi Aguchem, Innocent Uzochukwu Okagu, Ekezie Matthew Okorigwe

et al.

Life Sciences, Journal Year: 2024, Volume and Issue: 351, P. 122823 - 122823

Published: June 11, 2024

Cardiovascular diseases (CVDs) are a leading cause of mortality worldwide, primarily affecting the heart and blood vessels, with atherosclerosis being major contributing factor to their onset. Epidemiological clinical studies have linked high levels low-density lipoprotein (LDL) emanating from distorted cholesterol homeostasis as its predisposing factor. Cholesterol homeostasis, which involves maintaining balance in body level, is mediated by several proteins or receptors, transcription factors, even genes, regulating influx (through dietary intake de novo synthesis) efflux (by conversion bile acids). Previous knowledge about CVDs management has evolved around modulating these receptors' activities through synthetic small molecules/antibodies, limited interest natural products. The central roles cholesteryl ester transfer protein (CETP), proprotein convertase subtilisin/kexin type 9 (PCSK9), cytochrome P450 family 7 subfamily A member 1 (CYP7A1), among other fostered growing scientific interests understanding more on regulatory potential drug targets. We present up-to-date contributions CETP, PCSK9, CYP7A1 toward CVDs, highlighting successes failures molecules/antibodies modulate activities. In recommendation for new direction improve cardiovascular health, we presented recent findings products (including functional food, plant extracts, phytochemicals, bioactive peptides, therapeutic carbohydrates) that also PCSK-9, CYP7A1, emphasized need research efforts redirected unraveling potentials at trial level CVD management.

Language: Английский

Citations

4
Moving from lipids to leukocytes: inflammation and immune cells in atherosclerosis DOI Creative Commons

Maxim E. Annink,

Jordan M. Kraaijenhof, Erik S.G. Stroes

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: Aug. 5, 2024

Atherosclerotic cardiovascular disease (ASCVD) is the most important cause of morbidity and mortality worldwide. While it traditionally attributed to lipid accumulation in vascular endothelium, recent research has shown that plaque inflammation an additional driver atherogenesis. Though clinical outcome trials utilizing anti-inflammatory agents have proven promising terms reducing ASCVD risk, imperative identify novel actionable targets are more specific atherosclerosis mitigate adverse effects associated with systemic immune suppression. To end, this review explores contributions various cells from innate adaptive system promoting mitigating by integrating findings experimental studies, high-throughput multi-omics technologies, epidemiological research.

Language: Английский

Citations

4
Bioorthogonal Raman and IR probes for live cell metabolomics: a library DOI Creative Commons
Wiktoria Korona, B. Orzechowska, Kacper Siąkała

et al.

Sensors and Actuators B Chemical, Journal Year: 2025, Volume and Issue: unknown, P. 137363 - 137363

Published: Jan. 1, 2025

Language: Английский

Citations

0
Statin use and longitudinal bone marrow lesion burden: analysis of knees without osteoarthritis from the Osteoarthritis Initiative study DOI
Kamyar Moradi, Bahram Mohajer, Ali Guermazi

et al.

Skeletal Radiology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 31, 2025

Language: Английский

Citations

0
Inhibiting MiR-33a-3p Expression Fails to Enhance ApoAI-Mediated Cholesterol Efflux in Pro-Inflammatory Endothelial Cells DOI Creative Commons
Kun Huang,

Achala Pokhrel,

Jing Echesabal-Chen

et al.

Medicina, Journal Year: 2025, Volume and Issue: 61(2), P. 329 - 329

Published: Feb. 13, 2025

Background and Objectives: Atherosclerosis is an inflammatory condition that results in cholesterol accumulating within vessel wall cells. Atherosclerotic cardiovascular disease the leading cause of mortality worldwide due to this being a major contributor myocardial infarctions cerebrovascular accidents. Research suggests accumulation occurring precisely arterial endothelial cells triggers atherogenesis exacerbates atherosclerosis. Furthermore, inflamed endothelium acts as catalyst for atherosclerotic development. Therefore, enhancing removal specifically pro-inflammatory may be potential treatment option While we have previously shown inhibiting microRNA guide strand miR-33a-5p increases both ABCA1 expression apoAI-mediated efflux, it unknown whether miR-33a-3p passenger causes similar atheroprotective effects. In study, what aimed test. Materials Methods: We used plasmid transfection knockdown cultured immortalized mouse aortic (iMAECs). compared efflux these iMAECs transfected with control plasmid. Results: The resulted significant increase mRNA expression. However, inhibition did not significantly protein iMAECs. Moreover, failed detect from knockdown. Conclusions: Our indicative alone does enhance ABCA1-dependent To gain any benefit endothelium, additional anti-atherogenic strategies would likely needed unison.

Language: Английский

Citations

0