Glomerular endothelium: A porous sieve and formidable barrier

Obeidat, Marya; Obeidat, Motaz; Ballermann, Barbara J.

doi:10.1016/j.yexcr.2012.02.032

Cited by 67 publications

(61 citation statements)

References 82 publications

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“…Only 0.06% of plasma albumin is normally filtered, even though the fenestrae in the glomerulus are much larger than the albumin molecules: this is probably because of a negatively charged covering glycocalyx [29]. Studies with lipid droplets have shown an exclusion zone 175 nm thick above the glomerular endothelial surface, which was thinned by heparinase, chondroitinase and hyaluronidase.…”

Section: Damage To the Endothelial Surface Layermentioning

confidence: 99%

“…Degradation of the endothelial surface layer increases the permeability of the glomerular capillary wall to albumin, but not Ficoll (uncharged albumin), indicating that disruption of the endothelial surface layer leads to a defect in charge selectivity [30]. Microalbuminuria is associated with systemic endothelial dysfunction and cardiovascular complications, even in non-diabetic patients with essential hypertension and in women with a history of pre-eclampsia [29].…”

Section: Damage To the Endothelial Surface Layermentioning

confidence: 99%

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The endothelial glycocalyx: a review of the vascular barrier

Alphonsus¹,

2014

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SummaryThe endothelial glycocalyx is an important part of the vascular barrier. The glycocalyx is intimately linked to the homoeostatic functions of the endothelium. Damage to the glycocalyx precedes vascular pathology. In the first part of this paper, we have reviewed the structure, physiology and pathology of the endothelial glycocalyx, based on a literature search of the past five years. In the second part, we have systematically reviewed interventions to protect or repair the glycocalyx. Glycocalyx damage can be caused by hypervolaemia and hyperglycaemia and can be prevented by maintaining a physiological concentration of plasma protein, particularly albumin.

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Section: Damage To the Endothelial Surface Layermentioning

confidence: 99%

Section: Damage To the Endothelial Surface Layermentioning

confidence: 99%

The endothelial glycocalyx: a review of the vascular barrier

Alphonsus¹,

2014

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“…12 Both types bring great pharmaceutical promise through their stability, solubility and unique binding loop topography, but, with variable binding domains with an average molecular mass of 12-13 kDa, they are rapidly cleared in vivo by glomerular filtration. 13 Substantial efforts to address the question of systemic half-life extension have included different strategies to counter unfavorable pharmacokinetic (PK) properties.…”

Section: Construction and Screening Of The Immunized Vnar Phage Librarymentioning

confidence: 99%

Improving the pharmacokinetic properties of biologics by fusion to an anti-HSA shark VNAR domain

Müller

Saunders

Grace

et al. 2012

mAbs

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“…Compared with the endothelial cells in most vascular beds, glomerular endothelial cells are extremely flat and perforated by dense arrays of transcellular pores, the fenestrae. This phenotype is critical for the high glomerular water and electrolyte permeability (145).…”

Section: Expression Of Trpc6 In Endothelial Cellsmentioning

confidence: 99%

Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology

Chaudhari

2016

Antioxidants & Redox Signaling

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Significance: Regulation of Ca 2+ signaling cascade by reactive oxygen species (ROS) is becoming increasingly evident and this regulation represents a key mechanism for control of many fundamental cellular functions. Canonical transient receptor potential (TRPC) 6, a member of Ca 2+ -conductive channel in the TRPC family, is widely expressed in kidney cells, including glomerular mesangial cells, podocytes, tubular epithelial cells, and vascular myocytes in renal microvasculature. Both overproduction of ROS and dysfunction of TRPC6 channel are involved in renal injury in animal models and human subjects. Although regulation of TRPC channel function by ROS has been well described in other tissues and cell types, such as vascular smooth muscle, this important cell regulatory mechanism has not been fully reviewed in kidney cells. Recent Advances: Accumulating evidence has shown that TRPC6 is a redox-sensitive channel, and modulation of TRPC6 Ca 2+ signaling by altering TRPC6 protein expression or TRPC6 channel activity in kidney cells is a downstream mechanism by which ROS induce renal damage. Critical Issues: This review highlights how recent studies analyzing function and expression of TRPC6 channels in the kidney and their response to ROS improve our mechanistic understanding of oxidative stress-related kidney diseases. Future Directions: Although it is evident that ROS regulate TRPC6-mediated Ca 2+ signaling in several types of kidney cells, further study is needed to identify the underlying molecular mechanism. We hope that the newly identified ROS/TRPC6 pathway will pave the way to new, promising therapeutic strategies to target kidney diseases such as diabetic nephropathy. Antioxid. Redox Signal. 25, 732-748.

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Glomerular endothelium: A porous sieve and formidable barrier

Cited by 67 publications

References 82 publications

The endothelial glycocalyx: a review of the vascular barrier

The endothelial glycocalyx: a review of the vascular barrier

Improving the pharmacokinetic properties of biologics by fusion to an anti-HSA shark VNAR domain

Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology

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