osteoarthritis/hypoxia

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Reciprocal activation of hypoxia-inducible factor (HIF)-2α and the zinc-ZIP8-MTF1 axis amplifies catabolic signaling in osteoarthritis.

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OBJECTIVE Hypoxia-inducible factor (HIF)-2α and the zinc-ZIP8-MTF1 axis in chondrocytes serve as catabolic regulators of osteoarthritic cartilage destruction by regulating the expression of catabolic factor genes. We explored possible crosstalk between these signaling pathways and its biological

Hypoxia and HIF-1alpha in osteoarthritis.

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We have previously shown that functional inactivation of hypoxia-inducible factor-1alpha (HIF-1alpha) in growth-plate chondrocytes will dramatically inhibit anaerobic energy generation and matrix synthesis. Using immunohistochemistry, we have now analyzed the spatial distribution of HIF-1alpha and

Does hypoxia-reperfusion injury occur in osteoarthritis of the temporomandibular joint?

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OBJECTIVE To determine the available evidence in the literature for whether hypoxia-reperfusion injury plays a role in the pathogenesis of joint diseases in general and of osteoarthritis (OA) of the temporomandibular joint (TMJ) in particular. METHODS The electronic databases CENTRAL, PubMed, and

[Expression of hypoxia-inducible factor-1α and vascular endothelial growth factor in the synovium of patients with osteoarthritis].

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OBJECTIVE To detect the expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in patients with osteoarthritis and investigate their roles in the synovial lesions of osteoarthritis. METHODS The expressions of HIF-1α and VEGF in the synovium were detected by

[The relationship between hypoxia-inducible factor-1α and cartilage degeneration in osteoarthritis: a review].

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Osteoarthritis is one of the most common diseases seen in clinical practice. Cartilage survives in the hypoxic microenvironment. Hypoxia-inducible factor-1α (HIF-1α) is a key nuclear transcription factor which mediates the hypoxic response of cells. HIF-1α gene is an important regulator for the

Reciprocal regulation by hypoxia-inducible factor-2α and the NAMPT-NAD(+)-SIRT axis in articular chondrocytes is involved in osteoarthritis.

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OBJECTIVE Hypoxia-inducible factor-2α (HIF-2α) transcriptionally upregulates Nampt in articular chondrocytes. NAMPT, which exhibits nicotinamide phosphoribosyltransferase activity, in turn causes osteoarthritis (OA) in mice by stimulating the expression of matrix-degrading enzymes. Here, we sought

The effect of oestrogen on mandibular condylar cartilage via hypoxia-inducible factor-2α during osteoarthritis development.

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Oestrogen and hypoxia inducible factor-2α (HIF2α) are key regulators in the pathogenesis of osteoarthritis (OA). However, the cellular interaction between oestrogen and HIF2α in articular cartilage during OA process remains unknown. Our previous study has revealed that high-physiological level of

Association between hypoxia-inducible factor-1a levels in serum and synovial fluid with the radiographic severity of knee osteoarthritis.

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Osteoarthritis (OA) is primarily characterized by articular cartilage degradation. Hypoxia-inducible factor-1a (HIF-1a), a subunit of the basic helix-loop-helix-containing PER-ARNT-SIM (PAS) domain transcription factors, plays a vital role in the survival of articular chondrocytes to the hostile

Expression of hypoxia-inducible factor-1α in synovial fluid and articular cartilage is associated with disease severity in knee osteoarthritis.

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The aim of the present study was to examine hypoxia-inducible factor 1α (HIF-1α) levels in the synovial fluid and articular cartilage of patients with primary knee osteoarthritis (OA) and to investigate their association with the severity of disease. A total of 36 patients with knee OA and ten

Hypoxic conditions increase hypoxia-inducible transcription factor 2alpha and enhance chondrogenesis in stem cells from the infrapatellar fat pad of osteoarthritis patients.

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Stem cells derived from the infrapatellar fat pad (IPFP) are a potential source of stem cells for the repair of articular cartilage defects. Hypoxia has been shown to improve chondrogenesis in adult stem cells. In this study we investigated the effects of hypoxia on gene expression changes and

Synovial proliferation differentially affects hypoxia in the joint cavities of rheumatoid arthritis and osteoarthritis patients.

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This study was performed to investigate whether synovial proliferation (SP) differentially affects hypoxia in the joint cavities of rheumatoid arthritis (RA) and osteoarthritis (OA) patients. Thirty RA and 42 OA patients who underwent synovitis assessment were classified into two groups based on the

Catabolic stress induces expression of hypoxia-inducible factor (HIF)-1 alpha in articular chondrocytes: involvement of HIF-1 alpha in the pathogenesis of osteoarthritis.

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Transcription factor hypoxia-inducible factor (HIF)-1 protein accumulates and activates the transcription of genes that are of fundamental importance for oxygen homeostasis - including genes involved in energy metabolism, angiogenesis, vasomotor control, apoptosis, proliferation, and matrix

NAMPT (visfatin), a direct target of hypoxia-inducible factor-2α, is an essential catabolic regulator of osteoarthritis.

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OBJECTIVE Hypoxia-inducible factor 2α (HIF-2α), encoded by Epas1, causes osteoarthritic cartilage destruction by regulating the expression of matrix-degrading enzymes. We undertook this study to explore the role of nicotinamide phosphoribosyltransferase (NAMPT or visfatin) in HIF-2α-mediated

miRNA-411 Regulates Chondrocyte Autophagy in Osteoarthritis by Targeting Hypoxia-Inducible Factor 1 alpha (HIF-1α).

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BACKGROUND Osteoarthritis (OA) is the most common joint disease and is characterized by the progressive degeneration of articular cartilage. The molecular basis of OA involves various factors and has not been fully clarified. Autophagy is a conserved catabolic process that involves cellular

Upregulated hypoxia inducible factor-1alpha and -2alpha pathway in rheumatoid arthritis and osteoarthritis.

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The pathogenesis of rheumatoid arthritis (RA) and osteoarthritis (OA) remains obscure, although angiogenesis appears to play an important role. We recently confirmed an overexpression of two angiogenic factors, namely vascular endothelial growth factor (VEGF) and platelet-derived endothelial cell

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