Potential role of leptin in angiogenesis: leptin induces endothelial cell proliferation and expression of matrix metalloproteinases in vivo and in vitro

Park, Hyun-Young; Kwon, Hyuck Moon; Lim, Hyunwoo; Hong, Bum–Kee; Lee, Ju Yong; Park, Byoung Eun; Jang, Yangsoo; Cho, Seung Yun; Kim, Hyun Seung

doi:10.1038/emm.2001.17

Cited by 401 publications

(262 citation statements)

References 13 publications

Supporting

Mentioning

234

Contrasting

Unclassified

Order By: Relevance

“…This process leads to the diapedesis of monocytes and initiates a vicious circle of adipogenesis and inflammation (41). Several adipokines have a direct effect on endothelial function, including leptin and adiponectin (42,43). Chemerin, a novel adipokine at the crossroad between inflammation and obesity, may possibly influence the vascular endothelium as well.…”

Section: Review Bruyndonckx Et Almentioning

confidence: 99%

Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

et al. 2016

View full text Add to dashboard Cite

Section: Review Bruyndonckx Et Almentioning

confidence: 99%

Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

et al. 2016

View full text Add to dashboard Cite

“…In addition to the proangiogenic function, leptin can enhance endothelial cell growth (Bouloumie et al, 1998;Sierra-Honigmann et al, 1998) and suppress apoptosis through a Bcl-2-dependent mechanism (Artwohl et al, 2002). The role of leptin in neovascularization is supported additionally by the observation that the hormone can increase the levels and activity of enzymes involved in angiogenesis, for example, matrix metalloproteinases (MMPs) 2 and 9 (Park et al, 2001;Kume et al, 2002).…”

Section: Leptin and Its Activitiesmentioning

confidence: 99%

Leptin and cancer

Garofalo

Surmacz

2005

Journal Cellular Physiology

539

484

View full text Add to dashboard Cite

The prevalence of obesity has markedly increased over the past two decades, especially in the industrialized countries. While the impact of excess body weight on the development of cardiac disease and diabetes has been well documented, the link between obesity and carcinogenesis is just being recognized. This review will focus on the link between leptin, a cytokine that is elevated in obese individuals, and cancer development. First, we briefly discuss the biological functions of leptin and its signaling pathways. Then, we summarize the effects of leptin on different cancer types in experimental cellular and animal models. Next, we analyze epidemiological data on the relationship between obesity and the presence of cancer or cancer risk in patients. Finally, leptin as a target for cancer treatment and prevention will be discussed.

show abstract

“…In vivo, leptin receptors are expressed in vascular cells and leptin signaling promotes atherosclerosis in mouse models (Park et al 2001). Leptin has been shown to enhance the proliferation of human aortic VSMCs and MMP-2 expression, with concomitant increased generation of intracellular ROS and activation of PKC, ERK1/2 and NF-κB.…”

Section: Vascular Smooth Muscle Proliferationmentioning

confidence: 99%

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Papaharalambus

Griendling

2007

Trends in Cardiovascular Medicine

285

220

View full text Add to dashboard Cite

The development of vascular disease has its origins in an initial insult to the vessel wall by biological or mechanical factors. The disruption of homeostatic mechanisms leads to alteration of the original architecture of the vessel and its biological responsiveness, contributing to acute or chronic diseases such as stroke, hypertension and atherosclerosis. Endothelial dysfunction, macrophage infiltration of the vessel wall, and proliferation and migration of smooth muscle cells all involve different types of reactive oxygen species, produced by various vessel wall components. Although basic science and animal research have clearly established the role of reactive oxygen species in the progression of vascular disease, the failure of clinical trials with antioxidant compounds has underscored the need for better antioxidant therapies and a more thorough understanding of the role of reactive oxygen species in cardiovascular physiology and pathology.The fundamental processes underlying the development of vascular diseases such as atherosclerosis, restenosis and hypertensive vascular remodeling have their origins in an initial insult to the vessel wall. Such an insult may arise from mechanical disruption that occurs during percutaneous coronary angioplasty or at regions of oscillatory shear stress, or it can result from biological causes, such as hypercholesterolemia, excess free radicals, diabetes, increased concentrations of plasma homocysteine, or infectious agents. Injury promotes disruption of the homeostatic mechanisms of the endothelial protective barrier, changing its natural properties, increasing its adhesiveness to leukocytes and altering its permeability. This endothelial dysfunction also leads to the formation of vasoactive molecules, which in turn induce inflammatory genes, inactivate nitric oxide (NO • ) and its protective functions, and activate matrix metalloproteinases, leading to extracellular matrix remodeling, and increased smooth muscle cell (VSMC) growth, migration and proliferation. Each of these processes contributes to thickening of the vessel wall or the formation of lesions that can lead to hypertension, acute myocardial infarction and stroke. Reactive Oxygen Species and Vascular InjuryIn the past decade a staggering amount of evidence implicates a common denominator, reactive oxygen species (ROS), in the development of most cardiovascular diseases (Figure 1). Superoxide (O 2 •− ) and hydrogen peroxide (H 2 O 2 ) are two of the most biologically important ROS in the cardiovascular system, and are produced in vascular cells by a number of oxidases, including the NADPH oxidases (Nox) and xanthine oxidase, lipoxygenases, cytochrome p450,

show abstract

Potential role of leptin in angiogenesis: leptin induces endothelial cell proliferation and expression of matrix metalloproteinases in vivo and in vitro

Cited by 401 publications

References 13 publications

Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

Leptin and cancer

Basic Mechanisms of Oxidative Stress and Reactive Oxygen Species in Cardiovascular Injury

Contact Info

Product

Resources

About