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Banach, Maciej; Nikolić, Dragana; Rizzo, Manfredi; Tóth, Peter P.

doi:10.1097/hco.0000000000000305

Cited by 16 publications

(3 citation statements)

References 53 publications

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“…Instead, they create a molecular susceptibility that, in the presence of hypercholesterolemia, increases macrophage cholesterol accumulation, a central event in atherogenesis. From this perspective, obesity/IR can be conceptualized as a perturbation that “sensitizes macrophages to atherogenic lipoproteins,” which may help to explain why type 2 diabetics generally require more aggressive cholesterol lowering to achieve therapeutic benefit ( Banach et al, 2016 ; Hoe and Hegele, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

“…In epidemiological studies, traditional risk factors, such as smoking, hypertension, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, total cholesterol, and triglyceride levels, do not explain the risk associated with CVD in type 2 diabetic patients ( Beckman et al, 2002 ; Gore et al, 2015 ; Haffner et al, 1998 ; Hayward et al, 2015 ). Moreover, intervention studies showed that increased mortality is observed even when plasma cholesterol levels are aggressively lowered with statin treatment, hypertension is controlled, or with aggressive glycemic control ( Banach et al, 2016 ; Gore et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

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Obesity and Insulin Resistance Promote Atherosclerosis through an IFNγ-Regulated Macrophage Protein Network

et al. 2018

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SUMMARY Type 2 diabetes (T2D) is associated with increased risk for atherosclerosis; however, the mechanisms underlying this relationship are poorly understood. Macrophages, which are activated in T2D and causatively linked to atherogenesis, are an attractive mechanistic link. Here, we use proteomics to show that diet-induced obesity and insulin resistance (obesity/IR) modulate a pro-atherogenic “macrophage-sterol-responsive-network” (MSRN), which, in turn, predisposes macrophages to cholesterol accumulation. We identify IFNγ as the mediator of obesity/IR-induced MSRN dysregulation and increased macrophage cholesterol accumulation and show that obesity/IR primes T cells to increase IFNγ production. Accordingly, myeloid cell-specific deletion of the IFNγ receptor (Ifngr1−/−) restores MSRN proteins, attenuates macrophage cholesterol accumulation and atherogenesis, and uncouples the strong relationship between hyperinsulinemia and aortic root lesion size in hypercholesterolemic Ldlr−/− mice with obesity/IR, but does not affect these parameters in Ldlr−/− mice without obesity/IR. Collectively, our findings identify an IFNγ-macrophage pathway as a mechanistic link between obesity/IR and accelerated atherogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Obesity and Insulin Resistance Promote Atherosclerosis through an IFNγ-Regulated Macrophage Protein Network

et al. 2018

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“…Finally, it needs to be noted that lipid profiling should be performed every 6–8 weeks until the achievement of target concentrations of different lipid fractions. The common practice in outpatient treatment, however, is based on fixed doses of statins without biochemical monitoring of treatment results [6, 32, 168]. …”

Section: Causes Of Ineffective Treatment Of Dyslipidaemiasmentioning

confidence: 99%

PoLA/CFPiP/PCS Guidelines for the Management of Dyslipidaemias for Family Physicians 2016

Banach¹,

Jankowski²,

Jóźwiak³

et al. 2017

aoms

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145

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Step‐by‐step diagnosis and management of the nocebo/drucebo effect in statin‐associated muscle symptoms patients: a position paper from the International Lipid Expert Panel (ILEP)

Penson

Bruckert

Marais

et al. 2022

J cachexia sarcopenia muscle

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Statin intolerance is a clinical syndrome whereby adverse effects (AEs) associated with statin therapy [most commonly statin-associated muscle symptoms (SAMS)] result in the discontinuation of therapy and consequently increase the risk of adverse cardiovascular outcomes. However, complete statin intolerance occurs in only a small minority of treated patients (estimated prevalence of only 3-5%). Many perceived AEs are misattributed (e.g. physical musculoskeletal injury and inflammatory myopathies), and subjective symptoms occur as a result of the fact that patients expect them to do so when taking medicines (the nocebo/drucebo effect)-what might be truth even for over 50% of all patients with muscle weakness/pain. Clear guidance is necessary to enable the optimal management of plasma in real-world clinical practice in patients who experience subjective AEs. In this Position Paper of the International Lipid Expert Panel (ILEP), we present a step-by-step patient-centred approach to the identification and management of SAMS with a particular focus on strategies to prevent and manage the nocebo/drucebo effect and to improve long-term compliance with lipid-lowering therapy.

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Cited by 16 publications

References 53 publications

Obesity and Insulin Resistance Promote Atherosclerosis through an IFNγ-Regulated Macrophage Protein Network

Obesity and Insulin Resistance Promote Atherosclerosis through an IFNγ-Regulated Macrophage Protein Network

PoLA/CFPiP/PCS Guidelines for the Management of Dyslipidaemias for Family Physicians 2016

Step‐by‐step diagnosis and management of the nocebo/drucebo effect in statin‐associated muscle symptoms patients: a position paper from the International Lipid Expert Panel (ILEP)

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