A tissue in the tissue: Models of microvascular plasticity

Jacobsen, Jens Christian Brings; Hornbech, Morten Sonne; Holstein‐Rathlou, Niels‐Henrik

doi:10.1016/j.ejps.2008.09.012

Cited by 17 publications

(12 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was shown that there was a network density threshold below which resistance to flow dramatically increased. In addition, simulating hypertension in a mature and already compromised network leads to further rarefaction [48].…”

Section: Hypertension As a Results Of Microvascular Dysfunctionmentioning

confidence: 99%

Microvascular Dysfunction: A Potential Mechanism in the Pathogenesis of Obesity‐associated Insulin Resistance and Hypertension

et al. 2011

View full text Add to dashboard Cite

The intertwined epidemics of obesity and related disorders such as hypertension, insulin resistance, type 2 diabetes, and subsequent cardiovascular disease pose a major public health challenge. To meet this challenge, we must understand the interplay between adipose tissue and the vasculature. Microvascular dysfunction is important not only in the development of obesity-related targetorgan damage but also in the development of cardiovascular risk factors such as hypertension and insulin resistance. The present review examines the role of microvascular dysfunction as an explanation for the associations among obesity, hypertension, and impaired insulin-mediated glucose disposal. We also discuss communicative pathways from adipose tissue to the microcirculation.

show abstract

Section: Hypertension As a Results Of Microvascular Dysfunctionmentioning

confidence: 99%

Microvascular Dysfunction: A Potential Mechanism in the Pathogenesis of Obesity‐associated Insulin Resistance and Hypertension

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Although still limited, there is emerging evidence that the developmental environment can influence capillary number or length/volume density in key organs such as skeletal muscle, pancreas, brain, and kidney (summarized in Table 1). The physical rarefaction reported ranges between 20% and 43% and is similar to that seen in humans with essential hypertension [130] and modeled in simulations of microvascular networks [73]. Capillary rarefaction in skeletal muscle in young rats (7 and 28 days) but not in fetal rats with programmed raised blood pressure associated with a maternal low protein diet suggests an early postnatal disruption in normal microvascular development [120].…”

Section: Developmental Origins Of Microvascular Dysfunctionmentioning

confidence: 89%

“…The simulations showed that there was a network density threshold below which resistance to flow dramatically increased. In addition, simulating hypertension in a mature and already compromised network leads to further rarefaction [73]. In essential hypertension in humans, at least 60% of the attenuated capillary recruitment during a postocclusive reactive hyperemia may be explained by a structural rarefaction and the rest by functional rarefaction [130].…”

Section: Microvascular Function In Cardiometabolic Diseasementioning

confidence: 99%

The Microcirculation: A Target for Developmental Priming

Clough

Norman

2011

Microcirculation

View full text Add to dashboard Cite

There is increasing evidence that the early life environment, of which nutrition is a key component, acts through developmental adaptations to set the capacity of cardiovascular and metabolic pathways, and ultimately the limits to physiological challenges in later life. Suboptimal maternal nutrition and fetal growth result in reduced microvascular perfusion and functional dilator capacity, which are strongly associated with later development of obesity, type 2 diabetes, and hypertension. These conditions are also linked to microvascular rarefaction and remodeling that together limit capillary recruitment, reduce exchange capacity and increase diffusion distances of metabolic substrates, and increase local and overall peripheral resistance. Changes in small vessel structure and function may be seen very early, long before the onset of overt cardiovascular and metabolic disease, and may thus be a target for early therapeutic and lifestyle intervention strategies. This article explores how a disadvantageous microvascular phenotype may result from perinatal priming and how developmental plasticity may become an important and additional risk determinant in susceptibility to cardiometabolic disease in adult life.

show abstract

“…Microvascular rarefaction (functional and/or structural) may condition not only tissue vascular density, but also the maturity of the network structure and resistance to flow[110, 111]. In the kidney, such mechanisms may result in loss of glomerular and peritubular capillaries, ultimately leading to renal tubular and generalized parenchymal injury associated with reductions in renal blood flow and glomerular filtration rate.…”

Section: Microvascular Dysfunction As Potential Instigator Of Renal Imentioning

confidence: 99%

Role of the Renal Microcirculation in Progression of Chronic Kidney Injury in Obesity

Chade¹,

Hall²

2016

Am J Nephrol

View full text Add to dashboard Cite

Background: Obesity is largely responsible for the growing incidence and prevalence of diabetes, cardiovascular and renal diseases. Current strategies to prevent and treat obesity and its consequences have been insufficient to reverse the ongoing trends. Lifestyle modification or pharmacological therapies often produce modest weight loss which is not sustained and recurrence of obesity is frequently observed, leading to progression of target organ damage in many obese subjects. Therefore, research efforts have focused not only on the factors that regulate energy balance, but also on understanding mechanisms of target organ injury in obesity. Summary and Key Message: Microvascular (MV) disease plays a pivotal role in progressive kidney injury from different etiologies such as hypertension, diabetes, and atherosclerosis, which are all important consequences of chronic obesity. The MV networks are anatomical units that are closely adapted to specific functions of nutrition and removal of waste in every organ. Damage of the small vessels in several tissues and organs has been reported in obesity and may increase cardio-renal risk. However, the mechanisms by which obesity and its attendant cardiovascular and metabolic consequences interact to cause renal MV injury and chronic kidney disease are still unclear, although substantial progress has been made in recent years. This review addresses potential mechanisms and consequences of obesity-induced renal MV injury as well as current treatments that may provide protection of the renal microcirculation and slow progressive kidney injury in obesity.

show abstract

A tissue in the tissue: Models of microvascular plasticity

Cited by 17 publications

References 53 publications

Microvascular Dysfunction: A Potential Mechanism in the Pathogenesis of Obesity‐associated Insulin Resistance and Hypertension

Microvascular Dysfunction: A Potential Mechanism in the Pathogenesis of Obesity‐associated Insulin Resistance and Hypertension

The Microcirculation: A Target for Developmental Priming

Role of the Renal Microcirculation in Progression of Chronic Kidney Injury in Obesity

Contact Info

Product

Resources

About