Intracellular accumulation of advanced glycation end products induces apoptosis via endoplasmic reticulum stress in chondrocytes (Q43803960)

27 November 2017

Intracellular accumulation of advanced glycation end products induces apoptosis via endoplasmic reticulum stress in chondrocytes (English)

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27 November 2017

endoplasmic reticulum

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author name string

Soichiro Yamabe

1

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27 November 2017

Jun Hirose

2

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27 November 2017

Yusuke Uehara

3

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27 November 2017

Tatsuya Okada

4

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27 November 2017

Nobukazu Okamoto

5

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27 November 2017

Kiyoshi Oka

6

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27 November 2017

Takuya Taniwaki

7

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27 November 2017

Hiroshi Mizuta

8

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27 November 2017

language of work or name

English

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publication date

1 March 2013

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27 November 2017

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27 November 2017

280

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27 November 2017

1617-1629

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27 November 2017

7

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Linkage of chondrocyte apoptosis and cartilage degradation in human osteoarthritis.

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Caspase inhibitors reduce severity of cartilage lesions in experimental osteoarthritis

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Chondrocyte apoptosis: a cause or consequence of osteoarthritis?

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Cell death in cartilage.

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Endoplasmic reticulum stress signaling in disease

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Mediators of endoplasmic reticulum stress-induced apoptosis

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Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress

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Enhanced apoptotic and reduced protective response in chondrocytes following endoplasmic reticulum stress in osteoarthritic cartilage.

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Risk factors for onset of osteoarthritis of the knee in older adults: a systematic review and meta-analysis.

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AGEing and osteoarthritis: a different perspective

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Accumulation of advanced glycation end products as a molecular mechanism for aging as a risk factor in osteoarthritis

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Induction of advanced glycation end products and alterations of the tensile properties of articular cartilage

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Accumulation of advanced glycation end products decreases collagen turnover by bovine chondrocytes

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Activation of receptor for advanced glycation end products in osteoarthritis leads to increased stimulation of chondrocytes and synoviocytes

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Effects of advanced glycation end products on the expression of COX-2, PGE2 and NO in human osteoarthritic chondrocytes

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Advanced glycation end products induce the expression of interleukin-6 and interleukin-8 by receptor for advanced glycation end product-mediated activation of mitogen-activated protein kinases and nuclear factor-κB in human osteoarthritis chondrocyt

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Immunohistochemical demonstration of -(carboxymethyl)lysine protein adducts in normal and osteoarthritic cartilage

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Immunohistochemical distribution of advanced glycation end products (AGEs) in human osteoarthritic cartilage

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Advanced glycation end-products induce cell cycle arrest and hypertrophy in podocytes

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Advanced glycation end products induce cell cycle arrest and proinflammatory changes in osteoarthritic fibroblast-like synovial cells

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The formation of intracellular glyceraldehyde-derived advanced glycation end-products and cytotoxicity

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Hepatocyte inflammation model for cytotoxicity research: fructose or glycolaldehyde as a source of endogenous toxins.

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Glycolaldehyde induces apoptosis in a human breast cancer cell line

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Critical role of methylglyoxal and AGE in mycobacteria-induced macrophage apoptosis and activation

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Glycolaldehyde induces growth inhibition and oxidative stress in human breast cancer cells

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Human neutrophils employ the myeloperoxidase-hydrogen peroxide-chloride system to convert hydroxy-amino acids into glycolaldehyde, 2-hydroxypropanal, and acrolein. A mechanism for the generation of highly reactive alpha-hydroxy and alpha,beta-unsatu

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Identification in human atherosclerotic lesions of GA-pyridine, a novel structure derived from glycolaldehyde-modified proteins

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Influence of the hepatic eukaryotic initiation factor 2alpha (eIF2alpha) endoplasmic reticulum (ER) stress response pathway on insulin-mediated ER stress and hepatic and peripheral glucose metabolism

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Gadd153 sensitizes cells to endoplasmic reticulum stress by down-regulating Bcl2 and perturbing the cellular redox state

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CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum

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TAGE (toxic AGEs) hypothesis in various chronic diseases

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N (epsilon)-(carboxymethyl)lysine protein adduct is a major immunological epitope in proteins modified with advanced glycation end products of the Maillard reaction

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Conventional antibody against Nepsilon-(carboxymethyl)lysine (CML) shows cross-reaction to Nepsilon-(carboxyethyl)lysine (CEL): immunochemical quantification of CML with a specific antibody

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ER and aging-Protein folding and the ER stress response

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ER stress and hormetic regulation of the aging process

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Nitric oxide-induced apoptosis in pancreatic beta cells is mediated by the endoplasmic reticulum stress pathway

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Akt1 in murine chondrocytes controls cartilage calcification during endochondral ossification under physiologic and pathologic conditions

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Basic methods in histopathology of joint tissues

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S-nitrosylated protein-disulphide isomerase links protein misfolding to neurodegeneration

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Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

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21 January 2018

Identifiers

DOI

10.1111/FEBS.12170

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27 November 2017

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