Plasma Purification Treatment Relieves the Damage of Hyperlipidemia to PBMCs

Zhang, Xiao Meng; Gu, Yan; Deng, Hao; Xu, Zheng; Zhong, Zihang; Lyu, Xia Jie; Jin, Hui; Yang, Xiu Hong

doi:10.3389/fcvm.2021.691336

Cited by 3 publications

(2 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Then, the corresponding secondary antibodies were incubated according to the source of primary antibodies, which were mouse and rabbit antibodies, respectively. Finally, the results were quantified by ImageJ software (Scion Corp., USA) [ 22 ].…”

Section: Methodsmentioning

confidence: 99%

Glucose fluctuation promotes cardiomyocyte apoptosis by triggering endoplasmic reticulum (ER) stress signaling pathway in vivo and in vitro

Liu

et al. 2022

Bioengineered

View full text Add to dashboard Cite

Glucose fluctuation is more harmful than sustained hyperglycemia, but the effect on cardiomyocyte apoptosis have not yet been clarified. In this study, we aim to identify the effect of glucose fluctuation on cardiomyocyte apoptosis and explore the underlying mechanism. Sprague-Dawley rats were intraperitoneally injected with streptozotocin (STZ) and divided into three groups: controlled diabetic group (C-STZ); uncontrolled diabetic group (U-STZ) and glucose fluctuated diabetic group (GF-STZ). After twelve weeks, echocardiography, Hematoxylin-eosin (HE) staining, and Masson staining were adopted to assess the cardiac function and pathological changes. TUNEL staining was used to detect apoptotic cells. Expressions of apoptosis-related proteins and key molecules in the endoplasmic reticulum (ER) stress pathway were determined via western blots. Further, primary cardiomyocytes incubated in different glucose conditions were treated with the inhibitor of ER stress to explore the causative role of ER stress in glucose fluctuation-induced cardiomyocyte apoptosis. In vivo , we demonstrated that glucose fluctuation promoted cardiomyocyte apoptosis, and were more harmful to cardiomyocytes than sustained hyperglycemia. Moreover, glucose fluctuation significantly triggered ER stress signaling pathway. In vitro , primary cardiomyocyte apoptosis induced by glucose fluctuation and the activation of ER stress were significantly attenuated by 4-PBA, which is an ER stress inhibitor. Above all, glucose fluctuation can promote cardiomyocyte apoptosis through triggering the ER stress signaling pathway in diabetic rats and in primary cardiomyocytes.

show abstract

Section: Methodsmentioning

confidence: 99%

Glucose fluctuation promotes cardiomyocyte apoptosis by triggering endoplasmic reticulum (ER) stress signaling pathway in vivo and in vitro

Liu

et al. 2022

Bioengineered

View full text Add to dashboard Cite

show abstract

“…Beside non-statin therapies, other therapeutic options have emerged to meet the need for reducing circulating LDL-C. Double-filtration plasmapheresis (DFPP) is a lowcost treatment used to decrease LDL-C concentrations in patients with dyslipidaemias, such as homozygous familial hypercholesterolemia (HoFH) (10). In their original publication, Zhang et al sought to investigate the potential effects of nondrug therapy with double-filtration plasmapheresis (DFPP) on lipid metabolism-, endoplasmic reticulum (ER) stress-, and apoptosis-related proteins in peripheral blood mononuclear cells (PBMCs) before and after lipid clearance in patients with hyperlipidemia (11). In line with a previous study that reported that lipid plasmapheresis reduced plasma PCSK9 levels (12), they show that DFPP induces the downregulation of PCSK9, CD36 and LDLR in PBMCs.…”

mentioning

confidence: 99%

Editorial: Highlights in Lipids in Cardiovascular Disease: 2021

Boucheniata

Tessier

Martel

2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

This collection highlights a selection of articles published in 2021 from the Lipids in Cardiovascular Disease section of Frontiers in Cardiovascular Medicine. Lipids such as cholesterol and triglycerides (TG) are key contributors to cardiovascular disease (CVD) (1). They are transported in association with proteins in the circulation. These so-formed lipoproteins are complex particles divided into several classes based on their size, apolipoprotein and lipid composition. Chylomicrons, chylomicron remnants, VLDL, IDL, LDL, HDL, and Lp (a) have a central core containing cholesterol esters and triglycerides surrounded by free cholesterol, phospholipids and apolipoproteins (2). In 1961, the epidemiological Framingham Study demonstrated the association between high blood cholesterol levels and CVD (3). The subsequent "cholesterol hypothesis" that raised proposed that LDL-cholesterol (LDL-C) is instrumental for the development of atherosclerosis, the main underlying cause of CVD. Specific classes of lipoproteins thus began to be identified as triggers in the inflammatory processes, thereby promoting blood vessel inflammation and cardiomyopathies (4).Lowering of LDL-C had become a target of interest in the reduction of the risk of myocardial infarction and other cardiovascular events (5). Hydroxymethylglutaryl-CoA reductase (HMG-CoA) reductase inhibitors, frequently referred to as "statins, " are the gold standard for the management of LDL-C. However, many patients develop adverse drug effects (ADEs) and are unable to tolerate cholesterol-lowering medication. This highlights the need for the development of drugs designed to target other lipid mediators beyond LDL-C in patients with statin intolerances or in whom a statin alone does not lower LDL-C sufficiently, for instance (6, 7). The 2018 American College of Cardiology (ACC) and American Heart Association (AHA) guideline indicated that the non-statin therapies of choice should be ezetimibe, bile acid sequestrants/resins, and PCSK9 inhibitors (8). In the first paper of this special issue, Bardolia et al. provide an insightful narrative review of non-statin therapies that are shown promising in reducing LDL-C, either as monotherapy or in combination therapy with statins or other non-statin medications (9). They emphasize on the pharmacokinetic, efficacy and safety profiles of drugs that either selectively inhibit cholesterol absorption by the intestine (e.g., ezetimibe), prevent de novo cholesterol synthesis in hepatocytes (e.g., bempedoic acid, BDA), or reduce proprotein convertase subtilisin/kexin type 9 (PCSK9) function by preventing its binding to the LDL receptors (e.g., alirocumab, evolocumab) or by inhibiting its production by the liver (e.g., inclisiran).

show abstract