scholarly journals Ascorbic Acid Ameliorates Corneal Endothelial Dysfunction and Enhances Cell Proliferation via the Noncanonical GLUT1-ERK Axis

2021 ◽  
Author(s):  
Yi-Jen Hsueh ◽  
Yaa-Jyuhn James Meir ◽  
Jui-Yang Lai ◽  
Chieh-Cheng Huang ◽  
Tsai-Te Lu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Ascorbic Acid ◽  
Endothelial Dysfunction ◽  
Corneal Endothelial Dysfunction

scholarly journals Ascorbic acid ameliorates corneal endothelial dysfunction and enhances cell proliferation via the noncanonical GLUT1-ERK axis

2021 ◽  
Vol 144 ◽  
pp. 112306
Author(s):  
Yi-Jen Hsueh ◽  
Yaa-Jyuhn James Meir ◽  
Jui-Yang Lai ◽  
Chieh-Cheng Huang ◽  
Tsai-Te Lu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Ascorbic Acid ◽  
Endothelial Dysfunction ◽  
Corneal Endothelial Dysfunction

Ascorbic Acid does not Improve Endothelium-Dependent Flow-mediated Dilatation of the Brachial Artery in Patients with Raynaud’s Phenomenon Secondary to Systemic Sclerosis

2003 ◽  
Vol 73 (1) ◽  
pp. 3-7 ◽  
Author(s):  
M. E. Mavrikakis ◽  
J. P. Lekakis ◽  
M. Papamichael ◽  
K. S. Stamatelopoulos ◽  
Ch. C. Kostopoulos ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Smooth Muscle ◽  
Systemic Sclerosis ◽  
Endothelial Dysfunction ◽  
Brachial Artery ◽  
Raynaud’S Phenomenon ◽  
Raynaud's Phenomenon ◽  
Water Soluble ◽  
Placebo Administration ◽  
Flow Mediated Dilatation

Previous studies have shown that patients with Raynaud’s phenomenon secondary to systemic sclerosis present abnormal endothelial function; the mechanisms responsible for the endothelial dysfunction are unknown but increased vascular oxidative stress could be a possible cause. The hypothesis that a potent water-soluble antioxidant can reverse endothelial dysfunction in these patients was tested in the present study. We examined 11 female patients with Raynaud’s phenomenon secondary to systemic sclerosis and ten healthy control women by ultrasound imaging of the brachial artery to assess flow-mediated (endothelium-dependent) and nitrate-induced (endothelium-independent) vasodilatation. Flow-mediated dilatation and nitrate-induced dilatation were significantly reduced in patients with Raynaud’s phenomenon, indicating abnormal endothelial and smooth muscle cell function. Patients with Raynaud’s phenomenon entered a double-blind, randomized, crossover placebo-controlled trial and received orally 2 g of ascorbic acid or placebo; vascular studies were repeated two hours after ascorbic acid or placebo administration. Flow-mediated dilatation did not improve after ascorbic acid (1.6 ± 2.2% to 2.2 ± 2.5%, ns) or placebo administration (1.2 ± 1,9% to 1.7 ± 1.4%, ns); also nitrate-induced dilatation was similar after ascorbic acid or placebo (16 ± 7.4% vs 17 ± 8%, ns), suggesting no effect of ascorbic acid on endothelial and vascular smooth muscle function. In conclusion, ascorbic acid does not reverse endothelial vasomotor dysfunction in the brachial circulation of patients with Raynaud’s phenomenon secondary to systemic sclerosis. The use of different antioxidants or different dosing of ascorbic acid may be required to show a beneficial effect on endothelial vasodilator function.

Cell Therapy for Corneal Endothelial Dysfunction

2015 ◽  
pp. 135-135
Author(s):  
Noriko Koizumi ◽  
Shigeru Kinoshita ◽  
Naoki Okumura
Keyword(s):  
Endothelial Dysfunction ◽  
Cell Therapy ◽  
Corneal Endothelial Dysfunction

ASCORBIC ACID, CELL PROLIFERATION, AND CANCER

The Lancet ◽  
1972 ◽  
Vol 299 (7749) ◽  
pp. 542 ◽  
Author(s):  
Ewan Cameron ◽  
Douglas Rotman
Keyword(s):  
Cell Proliferation ◽  
Ascorbic Acid

scholarly journals Corneal endothelial cell dysfunction: etiologies and management

2018 ◽  
Vol 10 ◽  
pp. 251584141881580 ◽  
Author(s):  
Sepehr Feizi
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Corneal Endothelial Cell ◽  
Endothelial Cell Dysfunction ◽  
Endothelial Keratoplasty ◽  
Corneal Endothelial Cells ◽  
Cell Dysfunction ◽  
Corneal Endothelial Dysfunction

A transparent cornea is essential for the formation of a clear image on the retina. The human cornea is arranged into well-organized layers, and each layer plays a significant role in maintaining the transparency and viability of the tissue. The endothelium has both barrier and pump functions, which are important for the maintenance of corneal clarity. Many etiologies, including Fuchs’ endothelial corneal dystrophy, surgical trauma, and congenital hereditary endothelial dystrophy, lead to endothelial cell dysfunction. The main treatment for corneal decompensation is replacement of the abnormal corneal layers with normal donor tissue. Nowadays, the trend is to perform selective endothelial keratoplasty, including Descemet stripping automated endothelial keratoplasty and Descemet’s membrane endothelial keratoplasty, to manage corneal endothelial dysfunction. This selective approach has several advantages over penetrating keratoplasty, including rapid recovery of visual acuity, less likelihood of graft rejection, and better patient satisfaction. However, the global limitation in the supply of donor corneas is becoming an increasing challenge, necessitating alternatives to reduce this demand. Consequently, in vitro expansion of human corneal endothelial cells is evolving as a sustainable choice. This method is intended to prepare corneal endothelial cells in vitro that can be transferred to the eye. Herein, we describe the etiologies and manifestations of human corneal endothelial cell dysfunction. We also summarize the available options for as well as recent developments in the management of corneal endothelial dysfunction.

Corneal endothelial dysfunction in Pearson syndrome

2011 ◽  
Vol 34 (1-2) ◽  
pp. 55-57 ◽  
Author(s):  
Shivani A. Kasbekar ◽  
Jose A. Gonzalez-Martin ◽  
Ayad E. Shafiq ◽  
Arvind Chandna ◽  
Colin E. Willoughby
Keyword(s):  
Endothelial Dysfunction ◽  
Pearson Syndrome ◽  
Corneal Endothelial Dysfunction
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