Gal-3 is a potential biomarker for spinal cord injury and Gal-3 deficiency attenuates neuroinflammation through ROS/TXNIP/NLRP3 signaling pathway
Published 2019 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Gal-3 is a potential biomarker for spinal cord injury and Gal-3 deficiency attenuates neuroinflammation through ROS/TXNIP/NLRP3 signaling pathway
Authors
Keywords
-
Journal
BIOSCIENCE REPORTS
Volume 39, Issue 12, Pages -
Publisher
Portland Press Ltd.
Online
2019-11-25
DOI
10.1042/bsr20192368
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Carbon monoxide releasing molecule-3 inhibits inflammasome activation: A potential therapy for spinal cord injury
- (2019) Juan Pablo de Rivero Vaccari EBioMedicine
- Absence of TXNIP in Humans Leads to Lactic Acidosis and Low Serum Methionine Linked to Deficient Respiration on Pyruvate
- (2019) Yurika Katsu-Jiménez et al. DIABETES
- TXNIP-mediated nuclear factor-κB signaling pathway and intracellular shifting of TXNIP in uric acid-induced NLRP3 inflammasome
- (2019) Seong-Kyu Kim et al. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Hyperbaric oxygen improves functional recovery of the injured spinal cord by inhibiting inflammation and glial scar formation
- (2019) Yue Zhou et al. AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITATION
- MicroRNA-135b alleviates MPP+-mediated Parkinson’s disease in in vitro model through suppressing FoxO1-induced NLRP3 inflammasome and pyroptosis
- (2019) Rong Zeng et al. JOURNAL OF CLINICAL NEUROSCIENCE
- TXNIP/Redd1 signalling and excessive autophagy: a novel mechanism of myocardial ischaemia/reperfusion injury in mice
- (2019) Chao Gao et al. CARDIOVASCULAR RESEARCH
- Silencing miR-21 induces polarization of astrocytes to the A2 phenotype and improves the formation of synapses by targeting glypican 6 via the signal transducer and activator of transcription-3 pathway after acute ischemic spinal cord injury
- (2019) Yanlin Su et al. FASEB JOURNAL
- Gal-3 Deficiency Suppresses Novosphyngobium aromaticivorans Inflammasome Activation and IL-17 Driven Autoimmune Cholangitis in Mice
- (2019) Aleksandar Arsenijevic et al. Frontiers in Immunology
- Role and regulation mechanism of Gal-3 in non-small cell lung cancer and its potential clinical therapeutic significance
- (2019) Xiao-Ning Jiang et al. CHEMICO-BIOLOGICAL INTERACTIONS
- Comparisons of motor and sensory abnormalities after lumbar and thoracic contusion spinal cord injury in male rats
- (2019) Wanru Duan et al. NEUROSCIENCE LETTERS
- Inflammasome: Its role in traumatic brain and spinal cord injury
- (2018) Keywan Mortezaee et al. JOURNAL OF CELLULAR PHYSIOLOGY
- Lack of Galectin-3 attenuates neuroinflammation and protects the retina and optic nerve of diabetic mice
- (2018) Henrique Rocha Mendonça et al. BRAIN RESEARCH
- Elevated Carbohydrate Response Element-Binding Protein Beta (ChREBPβ) and Thioredoxin Interacting Protein (TXNIP) Levels in Human Adipocytes Differentiated in High Glucose Concentrations
- (2018) Vian Peshdary et al. Canadian Journal of Diabetes
- Plasma galectin-3 concentrations in patients with primary aldosteronism
- (2017) T.N.A. (Daniëlle) van den Berg et al. JOURNAL OF HYPERTENSION
- Galectin-3 Plays an Important Pro-inflammatory Role in the Induction Phase of Acute Colitis by Promoting Activation of NLRP3 Inflammasome and Production of IL-1β in Macrophages
- (2016) Bojana Simovic Markovic et al. Journal of Crohns & Colitis
- Deletion of galectin-3 exacerbates microglial activation and accelerates disease progression and demise in a SOD1G93Amouse model of amyotrophic lateral sclerosis
- (2012) Bruce J. Lerman et al. Brain and Behavior
Publish scientific posters with Peeref
Peeref publishes scientific posters from all research disciplines. Our Diamond Open Access policy means free access to content and no publication fees for authors.
Learn MoreCreate your own webinar
Interested in hosting your own webinar? Check the schedule and propose your idea to the Peeref Content Team.
Create Now