The Role of Statins in Current Guidelines

Rached, Fabiana; Santos, Raúl D.

doi:10.1007/s11883-020-00861-9

Cited by 21 publications

(12 citation statements)

References 82 publications

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“…It has been proved that a high level of LDL-C is a key risk factor for ASCVD [ 42 ]. Many clinical guidelines have shown that statins lower the incidence of ASCVD by reducing the levels of LDL-C, lipid content of plaques, and FCT [ 43 , 44 ]. Patients with low level of LDL-C who were treated with statins had a higher prevalence of calcification, which means that statins may help to prevent plaque rupture by calcification [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

Association between apolipoprotein B/A1 ratio and coronary plaque vulnerability in patients with atherosclerotic cardiovascular disease: an intravascular optical coherence tomography study

Deng

Lei

et al. 2021

Cardiovasc Diabetol

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Background Apolipoprotein (Apo) A1 and Apo B are strongly associated with the risk of atherosclerotic cardiovascular disease (ASCVD). However, the relationship between the Apo B/A1 ratio and the morphology of coronary vulnerable plaques has not been fully elucidated in patients with ASCVD. Methods A total of 320 patients with ASCVD undergoing percutaneous coronary intervention were enrolled and assigned into acute coronary syndrome (ACS) or chronic coronary syndrome (CCS) group. The morphology of culprit plaque was analyzed by intravascular optical coherence tomography. Association between the Apo B/A1 ratio and coronary vulnerable plaques were evaluated using logistic regression models and receiver operator characteristic (ROC) curve analyses. Results The Apo B/A1 ratio was higher in ACS patients than CCS patients (0.77 ± 0.28 vs. 0.64 ± 0.22, P < 0.001) and it was also higher in patients with plaque rupture, erosion or thrombus than those without culprit plaques. The high Apo B/A1 ratio was associated with high percent of vulnerable plaques compared with low ratio group. The Apo B/A1 ratio was negatively related to fibrous cap thickness in lipid-rich plaque (r = − 0.228, P = 0.043). Univariate and multivariate logistic regression analyses revealed that the Apo B/A1 ratio was an independent factor of plaque rupture, erosion, and thrombus. The area under the ROC curve of the Apo B/A1 ratio for plaque rupture, erosion, and thrombus were 0.632, 0.624, and 0.670 respectively (P < 0.001 for all), which were higher than that of low-density lipoprotein cholesterol. Conclusions The Apo B/A1 ratio is an independent predictor for plaque rupture, erosion, and thrombus in patients with ASCVD.

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Section: Discussionmentioning

confidence: 99%

Association between apolipoprotein B/A1 ratio and coronary plaque vulnerability in patients with atherosclerotic cardiovascular disease: an intravascular optical coherence tomography study

Deng

Lei

et al. 2021

Cardiovasc Diabetol

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“…Newer statins, including atorvastatin and rosuvastatin, have increased potency for lowering LDL-C and may achieve the desired LDL-C reduction more safely [ 106 ]. Statins remain an important component of atherosclerotic cardiovascular disease prevention and remain among the top-selling class of drugs worldwide [ 107 , 108 ].…”

Section: Current Lipid-lowering Treatments For Atherosclerosis: Succe...mentioning

confidence: 99%

Translating atherosclerosis research from bench to bedside: navigating the barriers for effective preclinical drug discovery

et al. 2022

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Cardiovascular disease (CVD) remains the leading cause of death worldwide. An ongoing challenge remains the development of novel pharmacotherapies to treat CVD, particularly atherosclerosis. Effective mechanism-informed development and translation of new drugs requires a deep understanding of the known and currently unknown biological mechanisms underpinning atherosclerosis, accompanied by optimization of traditional drug discovery approaches. Current animal models do not precisely recapitulate the pathobiology underpinning human CVD. Accordingly, a fundamental limitation in early-stage drug discovery has been the lack of consensus regarding an appropriate experimental in vivo model that can mimic human atherosclerosis. However, when coupled with a clear understanding of the specific advantages and limitations of the model employed, preclinical animal models remain a crucial component for evaluating pharmacological interventions. Within this perspective, we will provide an overview of the mechanisms and modalities of atherosclerotic drugs, including those in the preclinical and early clinical development stage. Additionally, we highlight recent preclinical models that have improved our understanding of atherosclerosis and associated clinical consequences and propose model adaptations to facilitate the development of new and effective treatments.

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“…This competition reduces the rate at which mevalonate is produced, thus inhibiting production of cholesterol in the liver [ 111 ]. In addition, statins also affect systemic cholesterol availability by promoting a compensatory decrease in circulating LDL and cholesterol transport through a variety of mechanisms [ 93 , 112 , 113 ]. The broad use of statins as first-line therapeutics for prevention of cardiovascular disease by inhibition of cholesterol synthesis raised the possibility of their effect on PCa.…”

Section: Effect Of a Class Of Drugs That Inhibit Cholesterol Synthesis On Prostate Cancer (Pca)mentioning

confidence: 99%

Inhibition of Scavenger Receptor Class B Type 1 (SR-B1) Expression and Activity as a Potential Novel Target to Disrupt Cholesterol Availability in Castration-Resistant Prostate Cancer

et al. 2021

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There have been several studies that have linked elevated scavenger receptor class b type 1 (SR-B1) expression and activity to the development and progression of castration-resistant prostate cancer (CRPC). SR-B1 facilitates the influx of cholesterol to the cell from lipoproteins in systemic circulation. This influx of cholesterol may be important for many cellular functions, including the synthesis of androgens. Castration-resistant prostate cancer tumors can synthesize androgens de novo to supplement the loss of exogenous sources often induced by androgen deprivation therapy. Silencing of SR-B1 may impact the ability of prostate cancer cells, particularly those of the castration-resistant state, to maintain the intracellular supply of androgens by removing a supply of cholesterol. SR-B1 expression is elevated in CRPC models and has been linked to poor survival of patients. The overarching belief has been that cholesterol modulation, through either synthesis or uptake inhibition, will impact essential signaling processes, impeding the proliferation of prostate cancer. The reduction in cellular cholesterol availability can impede prostate cancer proliferation through both decreased steroid synthesis and steroid-independent mechanisms, providing a potential therapeutic target for the treatment of prostate cancer. In this article, we discuss and highlight the work on SR-B1 as a potential novel drug target for CRPC management.

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The Role of Statins in Current Guidelines

Cited by 21 publications

References 82 publications

Association between apolipoprotein B/A1 ratio and coronary plaque vulnerability in patients with atherosclerotic cardiovascular disease: an intravascular optical coherence tomography study

Association between apolipoprotein B/A1 ratio and coronary plaque vulnerability in patients with atherosclerotic cardiovascular disease: an intravascular optical coherence tomography study

Translating atherosclerosis research from bench to bedside: navigating the barriers for effective preclinical drug discovery

Inhibition of Scavenger Receptor Class B Type 1 (SR-B1) Expression and Activity as a Potential Novel Target to Disrupt Cholesterol Availability in Castration-Resistant Prostate Cancer

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