Lipid lowering therapy in cardiovascular disease: From myth to molecular reality

Mourikis, Philipp; Zako, Saif; Dannenberg, Lisa; Nia, Amir M.; Heinen, Yvonne; Busch, Lucas; Richter, Hannah; Hohlfeld, Thomas; Zeus, Tobias; Kelm, Malte; Polzin, Amin

doi:10.1016/j.pharmthera.2020.107592

Cited by 40 publications

(23 citation statements)

References 109 publications

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“…Atherosclerosis is widely considered a lipid metabolism disorder (Gkretsi et al, 2011). Although many therapeutic agents, such as statins and evinacumab, have been successfully used for the treatment of atherosclerosis, the development of novel targets to fulfill unmet clinic requirements is still urgent (Mourikis et al, 2020; Yang et al, 2020). Macrophage‐derived foam cell formation is the hallmark of atherosclerotic lesion development (Wang et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐328‐5p Alleviates Macrophage Lipid Accumulation through the Histone Deacetylase 3/ATP‐binding cassette transporter A1 pathway

Huang

Jiang

et al. 2021

Lipids

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MicroRNA‐328 (miR‐328) was reported to protect against atherosclerosis, but its role in foam cell formation remains unknown. The aim of this study was to investigate the effect of miR‐328‐5p on macrophage lipid accumulation and the underlying mechanisms. The results showed that miR‐328‐5p expression was robustly decreased in oxidized low‐density lipoprotein (ox‐LDL)‐treated macrophages. Treatment of human acute monocytic leukemia cel (THP‐1) macrophage‐derived foam cells with a miR‐328‐5p mimic markedly increased [3H]‐cholesterol efflux, inhibited lipid droplet accumulation, and decreased intracellular total cholesterol (TC), free cholesterol (FC) and cholesteryl ester (CE) contents. Upregulation of miR‐328‐5p also reduced the expression of histone deacetylase 3 (HDAC3) but increased the levels of ATP‐binding cassette transporter A1 (ABCA1) in THP‐1 macrophage‐derived foam cells. Mechanistically, miR‐328‐5p inhibited HDAC3 expression by directly targeting its 3′UTR, thereby promoting ABCA1 expression and the subsequent cholesterol efflux. Furthermore, miR‐328‐5p mimic treatment did not affect the uptake of Dil‐ox‐LDL or the expression of scavenger receptor‐A (SR‐A), thrombospondin receptor (CD36) and ABCG1. Taken together, these findings suggest that miR‐328‐5p alleviates macrophage lipid accumulation through the HDAC3/ABCA1 pathway.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐328‐5p Alleviates Macrophage Lipid Accumulation through the Histone Deacetylase 3/ATP‐binding cassette transporter A1 pathway

Huang

Jiang

et al. 2021

Lipids

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“…Dyslipidemia has been shown to be associated with the efficacy and sensitivity of chemotherapeutic treatment (10). In addition, dyslipidemia can trigger cardiovascular diseases in breast cancer patients (11)(12)(13)(14). Therefore, blood lipids need to be closely monitored and managed in patients undergoing adjuvant chemotherapy for breast cancer.…”

Section: Effect Of Postoperative Chemotherapy On Blood Lipids In Patients With Invasive Breast Cancermentioning

confidence: 99%

Effect of postoperative chemotherapy on blood glucose and lipid metabolism in patients with invasive breast cancer

Qi¹,

Li²,

Yan³

et al. 2021

Gland Surg

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“…Coronary artery disease (CHD), peripheral artery disease (PAD), and atherosclerotic cerebrovascular disease represent major consequences of atherosclerosis, with atherosclerosis-induced cardiovascular disease accounting for substantial clinical and economic burdens [ 1 , 2 ]. While targeting elevated serum levels of low-density lipoprotein cholesterol (LDL) has been the mainstay of atherosclerosis prevention and treatment for decades, the evidence regarding the atherogenic role of hypertriglyceridemia is still controversial [ 3 ].…”

Section: Epidemiological Backgroundmentioning

confidence: 99%

Triglyceride-Rich Lipoproteins and Their Remnants as Silent Promoters of Atherosclerotic Cardiovascular Disease and Other Metabolic Disorders: A Review

Sascău

Clément²,

Radu

et al. 2021

Nutrients

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While targeting elevated serum levels of low-density lipoprotein cholesterol has been the mainstay of atherosclerosis prevention and treatment for decades, the evidence regarding the atherogenic role of hypertriglyceridemia is still controversial. Various epidemiological population-based studies on statin-treated subjects nominated triglycerides, triglyceride-rich lipoproteins (namely, chylomicrons and very-low-density lipoprotein particles), and their remnants as major determinants of the substantial residual cardiovascular risk. With the triglyceride-glucose index and triglyceride to high-density lipoprotein ratio emerging as surrogate indicators of peripheral artery disease and atherosclerotic cerebrovascular disease, one can conclude that further research addressing the intricate relationship between triglycerides and atherosclerosis is warranted. Therefore, this review aims to provide insight into the current clinical and epidemiological state of knowledge on the relationship between triglycerides and atherosclerotic cardiovascular disease. It also intends to highlight the connection between triglycerides and other metabolic disorders, including diabetes mellitus, and the potential benefits of triglyceride-lowering agents on cardiovascular outcomes and all-cause mortality.

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Lipid lowering therapy in cardiovascular disease: From myth to molecular reality

Cited by 40 publications

References 109 publications

MicroRNA‐328‐5p Alleviates Macrophage Lipid Accumulation through the Histone Deacetylase 3/ATP‐binding cassette transporter A1 pathway

MicroRNA‐328‐5p Alleviates Macrophage Lipid Accumulation through the Histone Deacetylase 3/ATP‐binding cassette transporter A1 pathway

Effect of postoperative chemotherapy on blood glucose and lipid metabolism in patients with invasive breast cancer

Triglyceride-Rich Lipoproteins and Their Remnants as Silent Promoters of Atherosclerotic Cardiovascular Disease and Other Metabolic Disorders: A Review

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