The BCR-ABL1 Inhibitors Imatinib and Ponatinib Decrease Plasma Cholesterol and Atherosclerosis, and Nilotinib and Ponatinib Activate Coagulation in a Translational Mouse Model

Pouwer, Marianne G.; Pieterman, Elsbet J.; Verschuren, Lars; Caspers, Martien P. M.; Kluft, C.; Garcia, Ricardo Alexandrino; Aman, Jurjan; Jukema, J. Wouter; Princen, H.M.G.

doi:10.3389/fcvm.2018.00055

Cited by 53 publications

(33 citation statements)

References 50 publications

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“…Both drugs, but ponatinib more potently, suppress endothelial function and induce endothelial apoptosis (54). In experimental models, ponatinib and nilotinib lead to changes consistent with increased plaque vulnerability (55). This might explain some, but not all of the pathophysiology seen with these medications.…”

Section: Predisposition To Thrombosis In Cancer Patientsmentioning

confidence: 99%

Arterial events in cancer patients—the case of acute coronary thrombosis

Ohad¹,

Herrmann²

2018

J. Thorac. Dis

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Patients with cancer are at high risk for both venous and arterial thrombotic complications. A variety of factors account for the greater thrombotic risk, including the underlying malignancy and numerous cancer-directed therapies. The occurrence of an acute thrombotic event in patients with cancer is associated with substantial morbidity and mortality. Acute coronary syndrome (ACS) represents a particularly important cardiovascular complication in cancer patients. With cardio-vascular risk factors becoming more prevalent in an aging cancer population that is surviving longer, questions pertaining to the appropriate management of vascular toxicity are likely to assume even greater value in the coming years. In this article, we review the current understanding of ACS in patients with cancer. The predisposition to thrombosis in a malignant host and the cancer treatments most commonly associated with vascular toxicity are reviewed. Risk prediction and management strategies are discussed, and discrepancies in the clinical evidence are highlighted.

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Section: Predisposition To Thrombosis In Cancer Patientsmentioning

confidence: 99%

Arterial events in cancer patients—the case of acute coronary thrombosis

Ohad¹,

Herrmann²

2018

J. Thorac. Dis

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“…However, only imatinib has a beneficial effect on the cardiovascular system, decreasing plasma cholesterol levels, reducing the atherosclerotic lesion, and improving plaque morphology. Ponatinib and nilotinib, on the other hand, increase the gene expression of coagulation factors VII and VIIa, revealing pronounce pro-thrombotic effects [125]. Imatinib was found to prevent macrophage transformation into foam cells by decreasing cholesterol levels.…”

Section: Pdgf Receptor Inhibitormentioning

confidence: 99%

Nanoparticle-Based Approaches towards the Treatment of Atherosclerosis

et al. 2020

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Atherosclerosis, being an inflammation-associated disease, represents a considerable healthcare problem. Its origin remains poorly understood, and at the same time, it is associated with extensive morbidity and mortality worldwide due to myocardial infarctions and strokes. Unfortunately, drugs are unable to effectively prevent plaque formation. Systemic administration of pharmaceuticals for the inhibition of plaque destabilization bears the risk of adverse effects. At present, nanoscience and, in particular, nanomedicine has made significant progress in both imaging and treatment of atherosclerosis. In this review, we focus on recent advances in this area, discussing subjects such as nanocarriers-based drug targeting principles, approaches towards the treatment of atherosclerosis, utilization of theranostic agents, and future prospects of nanoformulated therapeutics against atherosclerosis and inflammatory diseases. The focus is placed on articles published since 2015 with additional attention to research completed in 2019–2020.

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“…Imatinib treatment also results in an improvement of insulin sensitivity and glucose disposal in insulin-resistant rats, but the mechanism behind this effect has not been established (Agerkvist et al, 2008). Additionally, treatment with imatinib in mice lowers cholesterol-induced atherosclerosis, although the mechanism for this effect is not clear (Pouwer et al, 2018). As PDGFR signaling inhibits adipogenesis, pharmacological blockade might enhance adipocyte differentiation in white adipose tissues (Fitter et al, 2012).…”

Section: Pdgf-a and Pdgf-bmentioning

confidence: 99%

Regulation of Energy Metabolism by Receptor Tyrosine Kinase Ligands

et al. 2020

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Integrative Physiology, a section of the journal Frontiers in PhysiologyMetabolic diseases, such as diabetes, obesity, and fatty liver disease, have now reached epidemic proportions. Receptor tyrosine kinases (RTKs) are a family of cell surface receptors responding to growth factors, hormones, and cytokines to mediate a diverse set of fundamental cellular and metabolic signaling pathways. These ligands signal by endocrine, paracrine, or autocrine means in peripheral organs and in the central nervous system to control cellular and tissue-specific metabolic processes. Interestingly, the expression of many RTKs and their ligands are controlled by changes in metabolic demand, for example, during starvation, feeding, or obesity. In addition, studies of RTKs and their ligands in regulating energy homeostasis have revealed unexpected diversity in the mechanisms of action and their specific metabolic functions. Our current understanding of the molecular, biochemical and genetic control of energy homeostasis by the endocrine RTK ligands insulin, FGF21 and FGF19 are now relatively well understood. In addition to these classical endocrine signals, non-endocrine ligands can govern local energy regulation, and the intriguing crosstalk between the RTK family and the TGFβ receptor family demonstrates a signaling network that diversifies metabolic process between tissues. Thus, there is a need to increase our molecular and mechanistic understanding of signal diversification of RTK actions in metabolic disease. Here we review the known and emerging molecular mechanisms of RTK signaling that regulate systemic glucose and lipid metabolism, as well as highlighting unexpected roles of non-classical RTK ligands that crosstalk with other receptor pathways.

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The BCR-ABL1 Inhibitors Imatinib and Ponatinib Decrease Plasma Cholesterol and Atherosclerosis, and Nilotinib and Ponatinib Activate Coagulation in a Translational Mouse Model

Cited by 53 publications

References 50 publications

Arterial events in cancer patients—the case of acute coronary thrombosis

Arterial events in cancer patients—the case of acute coronary thrombosis

Nanoparticle-Based Approaches towards the Treatment of Atherosclerosis

Regulation of Energy Metabolism by Receptor Tyrosine Kinase Ligands

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