Vascular Endothelial Growth Factors

Ylä‐Herttuala, Seppo; Rissanen, Tuomas T.; Vajanto, Ismo; Hartikainen, Juha

doi:10.1016/j.jacc.2006.09.053

Cited by 412 publications

(141 citation statements)

References 90 publications

(145 reference statements)

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“…VEGF plays an important role in angiogenesis, endothelial cell survival, vasodilatation, and cardiac contractile function. 42 Thus, on-target cardiovascular effects of VEGF-targeted angiogenesis inhibitors such as increased blood pressure 43 are expected. Other toxicities that are at least in part caused by on-target effects include promotion of thromboembolism and cardiac contractile dysfunction.…”

Section: Trastuzumab and Her2-targeted Agentsmentioning

confidence: 99%

Cardio-Oncology

Lenneman

Sawyer

2016

Circulation Research

350

138

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Through the success of basic and disease-specific research, cancer survivors are one of the largest growing subsets of individuals accessing the healthcare system. Interestingly, cardiovascular disease is the second leading cause of morbidity and mortality in cancer survivors after recurrent malignancy. This recognition has helped stimulate a collaboration between oncology and cardiology practitioners and researchers, and the portmanteau cardio-oncology (also known as onco-cardiology) can now be found in many medical centers. This collaboration promises new insights into how cancer therapies impact cardiovascular homeostasis and long-term effects on cancer survivors. In this review, we will discuss the most recent views on the cardiotoxicity related to various classes of chemotherapy agents and radiation. We will also discuss broadly the current strategies for treating and preventing cardiovascular effects of cancer therapy.

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Section: Trastuzumab and Her2-targeted Agentsmentioning

confidence: 99%

Cardio-Oncology

Lenneman

Sawyer

2016

Circulation Research

350

138

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“…However, VEGF production is also known to be stimulated by hypoxia [54], and its enhanced expression has been observed in skeletal muscles that are severely ischaemic and undergo inflammatory regeneration [46]. As such, it has been widely viewed as a key mediator of ischaemia-induced angiogenesis in muscle [55], activated via hypoxic transcription factor HIF-1α or HIF-independent transcriptional coactivator PCG-1 [56]. During the development of mild-to-moderate ischaemia in the model of iliac artery ligation, resting blood flow decreased to 30–40% of the control values after 3 days and, although it gradually increased, was still lower than in controls 5 weeks later.…”

Section: Adaptation Of the Microvascular Bed To Decreased Blood Flowmentioning

confidence: 99%

Adaptation of Skeletal Muscle Microvasculature to Increased or Decreased Blood Flow: Role of Shear Stress, Nitric Oxide and Vascular Endothelial Growth Factor

Hudlická¹,

Brown

2009

J Vasc Res

119

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This review elucidates the roles of capillary haemodynamics, nitric oxide (NO) and vascular endothelial growth factor (VEGF) in the remodelling of skeletal muscle microcirculation in response to increased (electrical stimulation) or decreased (chronic ischaemia) blood flow. During early stages of stimulation-induced angiogenesis, up-regulation of VEGF and its receptor VEGF receptor 2 is dependent on shear stress and NO release, whereas later, involvement of NO in the expanding capillary bed appears to be VEGF/VEGF receptor 2 independent. Arteriolar growth most likely relies on mechanical wall stresses while growth factor involvement is less clear. By contrast, in muscles with restricted blood flow, increased VEGF/VEGF receptor 2 expression after ischaemia onset is not associated with changes in shear stress or hypoxia, or capillary growth. After several weeks, VEGF protein levels are lower than normal while modest angiogenesis takes place, a temporal mismatch that limits the utility of using growth factor levels during ischaemia to assess angiogenic potential. Chronic stimulation of ischaemic muscles restores their depressed endothelial-dependent arteriolar dilatation, increases capillary shear stress and VEGF receptor 2 and promotes capillary growth. In patients with peripheral vascular disease, electrical stimulation of ischaemic calf muscles increases blood flow, capillary surface area and muscle performance, offering an alternative ‘endogenous’ treatment to gene or cell therapy.

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“…Increased amounts of VEGF were detected additionally in PD patients described in the literature [14]. VEGF is a member of a family covering VEGF-A, VEGF-B, VEGF-C, VEGF-D, and placental growth factor (PIGF) [15]. But indeed VEGF-A is the most important member regarding pathology and should represent almost all stainable molecules in our investigation.…”

Section: Discussionmentioning

confidence: 82%

Fibrogenic Growth Factors in Encapsulating Peritoneal Sclerosis

et al. 2009

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Background: Increased local levels of fibrogenic growth hormones contribute substantially to the process of encapsulating peritoneal sclerosis (EPS) in animal models. Methods: We analyzed probes from patients with normal kidney function (n = 10), with normal kidney function and inflammation (n = 10), on PD without (n = 10) and with EPS (n = 9). We investigated the degree of fibrosis and the number of vessels and vasculopathy. Additionally, we investigated the expression of NFκB, TGFβ1, TGFβ1 receptor, TGFβ2, TGFβ2 receptor, FGF-BP, CTGF and VEGF by immunohistochemistry. Results: In EPS, we found an exclusive upregulation of VEGF (normal 0, appendicitis 1.0 ± 1.2, PD 1.7 ± 1.8 and EPS 5.7 ± 4.4; p < 0.0001), whereas in PD, CTGF was significantly increased (normal 6.0 ± 2.8, appendicitis 7.3 ± 2.5, PD 10.0 ± 1.8 and EPS 7.3 ± 2.1; p = 0.0059). The results for the TGFβ system and NFκB were not uniform, in EPS no increases were demonstrable. Vasculopathy was significantly more pronounced in EPS (normal 0.4 ± 0.5, appendicitis 0.2 ± 0.3, PD 1.0 ± 0.7 and EPS 1.6 ± 1.2; p < 0.0001) than in PD or inflammation (normal 30 ± 16, appendicitis 82 ± 48, PD 1,936 ± 952 and EPS 2,613 ± 1,209; p < 0.0001), whereas the density of vessels were decreased (normal 125 ± 114, appendicitis 817 ± 347, PD 81 ± 57 and EPS 36 ± 33; p < 0.0001). Conclusions: The process of EPS was associated with increased VEGF in the peritoneum. The reduced density of vessels compared with marked fibrosis could point to hypoxia as an inducer.

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Vascular Endothelial Growth Factors

Cited by 412 publications

References 90 publications

Cardio-Oncology

Cardio-Oncology

Adaptation of Skeletal Muscle Microvasculature to Increased or Decreased Blood Flow: Role of Shear Stress, Nitric Oxide and Vascular Endothelial Growth Factor

Fibrogenic Growth Factors in Encapsulating Peritoneal Sclerosis

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