Decreased blood oxygen diffusion in hypercholesterolemia

Menchaca, Hector J.; Michalek, Van N.; Rohde, Thomas D.; O'Dea, Thomas J.; Buchwald, Hēnry

doi:10.1067/msy.1998.90944

Cited by 20 publications

(19 citation statements)

References 16 publications

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“…The view of high-cholesterol cell membranes as a barrier is further affirmed in studies of red blood cell (RBC) oxygenation by Buchwald and colleagues [2, 3]. Specifically, the rate of oxygen uptake and release declines with the plasma membrane cholesterol content of RBCs [3].…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, the rate of oxygen uptake and release declines with the plasma membrane cholesterol content of RBCs [3]. As a result, RBC oxygen saturation is diminished, and oxygen release upon demand is diminished [2].…”

Section: Introductionmentioning

confidence: 99%

“…As a result, RBC oxygen saturation is diminished, and oxygen release upon demand is diminished [2]. The authors propose that angina pectoris in patients with hypercholesterolemia may be caused partly by reduced oxygen release from RBCs with elevated membrane cholesterol, contributing to heart muscle hypoxia and painful lactic acid buildup [3]. …”

Section: Introductionmentioning

confidence: 99%

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Magnification of Cholesterol-Induced Membrane Resistance on the Tissue Level: Implications for Hypoxia

Shea

Smith

Pias

2016

Advances in Experimental Medicine and Biology

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High cellular membrane cholesterol is known to generate membrane resistance and reduce oxygen (O2) permeability. As such, cholesterol may contribute to the Warburg effect in tumor cells by stimulating intracellular hypoxia that cannot be detected from extracellular oxygen measurements. We probe the tissue- level impact of the phenomenon, asking whether layering of cells can magnify the influence of cholesterol, to modulate hypoxia in relation to capillary proximity. Using molecular dynamics simulations, we affirm that minimally hydrated, adjacent lipid bilayers have independent physical behavior. Combining this insight with published experimental data, we predict linearly increasing impact of membrane cholesterol on oxygen flux across cells layered in tissue.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Magnification of Cholesterol-Induced Membrane Resistance on the Tissue Level: Implications for Hypoxia

Shea

Smith

Pias

2016

Advances in Experimental Medicine and Biology

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“…This produces a greater barrier to oxygen diffusion that both delays oxygen entry into the erythrocyte during saturation and delays oxygen release during desaturation. [18][19][20] Indeed, the percentage change in blood oxygen diffusion has been found to be inversely proportional to plasma cholesterol concentration. 18 Consequently, cholesterol contributes to renal hypoxia by reducing the erythrocyte capacity to both load and release oxygen.…”

Section: Hypertensionmentioning

confidence: 99%

“…This in turn is driven by a constellation of interlinked risk factors. Primary amongst these factors are anemia, [6][7][8][9] diabetic hyperglycemia, [10][11][12] hypertension, [13][14][15][16][17] hypercholesterolemia, [18][19][20] cigarette smoking, [21][22][23][24][25][26][27] air pollution, [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] atherosclerosis, [43][44][45][46][47][48][49][50][51][52] repeated episodes of acute kidney injury, [53][54][55][56]…”

mentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

125

111

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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Discerning Membrane Steady-State Oxygen Flux by Monte Carlo Markov Chain Modeling

Angles¹,

Pias²

2021

Advances in Experimental Medicine and Biology

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Decreased blood oxygen diffusion in hypercholesterolemia

Cited by 20 publications

References 16 publications

Magnification of Cholesterol-Induced Membrane Resistance on the Tissue Level: Implications for Hypoxia

Magnification of Cholesterol-Induced Membrane Resistance on the Tissue Level: Implications for Hypoxia

Hypoxia: The Force that Drives Chronic Kidney Disease

Discerning Membrane Steady-State Oxygen Flux by Monte Carlo Markov Chain Modeling

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