Editorial commentary: The lower the LDL the better but how and how much?

Gitin, Alexander; Pfeffer, Marc A.; Hennekens, Charles H.

doi:10.1016/j.tcm.2018.01.008

Cited by 4 publications

(2 citation statements)

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“…Considering the aforementioned pathogenesis, lowering LDL levels is currently considered a basic treatment approach for atherosclerosis in clinical practice. Although effective methods including statins and preprotein invertase Bacillus subtilis invertase/Kexin9 (PCSK9) inhibitors inhibit the levels of circulating LDL to a certain extent, they have been linked to various adverse cardiovascular events, threatening the lives of patients [ 21 ]. For instance, a 2017 CANTOS trial [ 22 ] revealed that although canakinumab, a monoclonal antibody that inhibits IL-1

reduced the incidence of adverse cardiovascular events (MACEs), it significantly exacerbated the incidence of coinfections and sepsis.…”

Section: Atherosclerosismentioning

confidence: 99%

NLRP3 Inflammasome as a Therapeutic Target for Atherosclerosis: A Focus on Potassium Outflow

Jin¹,

An²,

Sun³

et al. 2022

Rev. Cardiovasc. Med.

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Atherosclerosis is a risk factor for various cardiovascular diseases, and is linked to high rates of morbidity and mortality across the globe. Although numerous complex processes are involved in the development and progression of atherosclerosis, the exact mechanisms behind its pathogenesis remain unclear. Inflammation and endothelial cell damage exert a lasting effect on atherosclerosis, causing lipid and fibrous tissue accumulation in the intima of the artery to form plaques, and subsequently promoting atherosclerosis. Nod-like receptor protein 3 (NLRP3) inflammatory corpuscle is thought to be the link between lipid metabolism and inflammation. Long Potassium outflow is a vital activator of NLRP3, with a simultaneous effect as a start-up and adjustment. The majority of existing drugs for atherosclerosis targeting the NLRP3 signaling pathway target IL-1, whereas drugs targeting the critical link of potassium efflux are relatively new. This review discusses the NLRP3 inflammatory corpuscle as a critical regulator of the immunological inflammatory pathway in atherosclerosis. Moreover, current knowledge on NLRP3 inflammatory corpuscle start and activation pathways were integrated, emphasizing potassiuminvolved outflow-related proteins. We highlight potential treatment approaches for NLRP3 inflammatory corpuscle pathways, specifically targeting potassium outflow channels of targeted drugs. Collectively, these insights indicate that targeting the NLRP3 inflammatory corpuscle is a vital anti-inflammatory therapy for treating atherosclerosis.

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reduced the incidence of adverse cardiovascular events (MACEs), it significantly exacerbated the incidence of coinfections and sepsis.…”

Section: Atherosclerosismentioning

confidence: 99%

NLRP3 Inflammasome as a Therapeutic Target for Atherosclerosis: A Focus on Potassium Outflow

Jin¹,

An²,

Sun³

et al. 2022

Rev. Cardiovasc. Med.

View full text Add to dashboard Cite

show abstract

“…Because of the wide body of evidence from clinical trials and from epidemiological, genetic, and experimental studies that consistently demonstrate that the lower the level of LDL-C, the lower the CVD risk, regardless of baseline LDL levels, an approach has emerged that lower LDL-C goals should be targeted, particularly for those in high CVD risk groups [2,3]. In the recently released ESC/EAS lipid guidelines, for example, there is a recommendation for a 50% or greater lowering of LDL-C and an LDL-C target of less than 55 mg/dL in very high risk CVD subjects [3].…”

mentioning

confidence: 99%