ArticleScientific reports2016
HtrA2 suppresses autoimmune arthritis and regulates activation of STAT3.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Tofacitinib blocks IFN-regulated biomarker genes in skin fibroblasts and keratinocytes in a systemic sclerosis trial.JCI insight · 2022Trial
- Exploration of novel β-lactamase inhibitors against Klebsiella pneumoniae using fragment-based drug discovery approach.Molecular diversity · 2026Article
- HTRA2/OMI-Mediated Mitochondrial Quality Control Alters Macrophage Polarization Affecting Systemic Chronic Inflammation.International journal of molecular sciences · 2024Review
- Absent in melanoma 2 (AIM2) in rheumatoid arthritis: novel molecular insights and implications.Cellular & molecular biology letters · 2022Review
- Stem cells differentiation into insulin-producing cells (IPCs): recent advances and current challenges.Stem cell research & therapy · 2022Review
- Caloric restriction overcomes pre-diabetes and hypertension induced by a high fat diet and renal artery stenosis.Molecular biology reports · 2022Article
- Role of ALDH1A1 and HTRA2 expression in CCL2/CCR2-mediated breast cancer cell growth and invasion.Biology open · 2019Article
- RIPK1 inhibition attenuates experimental autoimmune arthritis via suppression of osteoclastogenesis.Journal of translational medicine · 2019Article
- The Therapeutic Effect of STAT3 Signaling-Suppressed MSC on Pain and Articular Cartilage Damage in a Rat Model of Monosodium Iodoacetate-Induced Osteoarthritis.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is an autoimmune disease that is related to the induction of T helper (Th)17 cells, which secrete interleukin-17, and activation of the signal transducer and activator of transcription (STAT) 3. The expression of high-temperature requirement protein A (HtrA) 2, a serine protease involved in apoptosis, was decreased in RA patients nonresponsive to drug treatment of RA. The aim of this study was to determine whether overexpression of HtrA2 has a therapeutic effect on RA. Th17 differentiation, osteoclastogenesis, and lymphocyte activation are increased in motor neuron degeneration (mnd)2 mice, which lack HtrA2 activity because of a missense mutation (Ser276Cys) in the protease domain of HtrA2. The inhibitor of HtrA2 also increased Th17 differentiation. On the other hand, HtrA2 induced cleavage of STAT3 and overexpression of HtrA2 attenuated CIA in a mouse model. HtrA2 overexpression inhibited plaque development as well as the differentiation of Th17 in ApoE
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