ArticleScientific reports2022
Bile acids attenuate PKM2 pathway activation in proinflammatory microglia.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- ENO1 interacts with PKM to promote HBV-related hepatocellular carcinoma progression and HBV replication.Journal of translational medicine · 2026Article
- Genistein-3'-sodium sulfonate improves neuroinflammation, blood-brain barrier function, and microglial activation after chronic cerebral hypoperfusion by regulating TGR5.Metabolic brain disease · 2026Article
- Beyond the gut: decoding the gut-immune-brain axis in health and disease.Cellular & molecular immunology · 2025Review
- THSG counteracts microglial glycolytic reprogramming and neuronal necroptosis both in vivo and in vitro under conditions of neuroinflammation.Scientific reports · 2025Article
- The role of gut microbiota-derived metabolites in neuroinflammation.Neuroprotection (Chichester, England) · 2025Review
- Evaluation of Additive Neuroprotective Effect of Combination Therapy for Parkinson's Disease Using In Vitro Models.Antioxidants (Basel, Switzerland) · 2025Article
- Diverse Physiological Roles of Kynurenine Pathway Metabolites: Updated Implications for Health and Disease.Metabolites · 2025Review
- PKM2 is a key factor to regulate neurogenesis and cognition by controlling lactate homeostasis.Stem cell reports · 2025Article
- Gut-Spinal Cord Axis in Spinal Cord Injury: Bidirectional Inflammatory Mechanisms and Microbiota-Targeted Therapeutic Strategies.Journal of inflammation research · 2025Review
- The Activation of PKM2 Induces Pyroptosis in Hippocampal Neurons via the NLRP3/Caspase-1/GSDMD Pathway in Neonatal Rats With Hypoxic-Ischemic Brain Injury.Brain and behavior · 2024Article
- Infection‑associated bile acid disturbance contributes to macrophage activation in patients with cirrhosis.Molecular medicine reports · 2024Article
- Emerging Roles of Bile Acids and TGR5 in the Central Nervous System: Molecular Functions and Therapeutic Implications.International journal of molecular sciences · 2024Review
- The Role of PKM2 in Multiple Signaling Pathways Related to Neurological Diseases.Molecular neurobiology · 2024Review
- Imbalance in Glucose Metabolism Regulates the Transition of Microglia from Homeostasis to Disease-Associated Microglia Stage 1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Gut Metabolites Acting on the Gut-Brain Axis: Regulating the Functional State of Microglia.Aging and disease · 2024Review
- Microbiota-gut-brain axis and its therapeutic applications in neurodegenerative diseases.Signal transduction and targeted therapy · 2024Review
- High-salt diet induces microbiome dysregulation, neuroinflammation and anxiety in the chronic period after mild repetitive closed head injury in adolescent mice.Brain communications · 2024Article
- Combination of tauroursodeoxycholic acid, co-enzyme Q10 and creatine demonstrates additive neuroprotective effects inFrontiers in neuroscience · 2024Article
- Connecting the Gut Microbiota and Neurodegenerative Diseases: the Role of Bile Acids.Molecular neurobiology · 2023Review
- Roles of bile acids signaling in neuromodulation under physiological and pathological conditions.Cell & bioscience · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Glycolysis is the metabolic pathway that converts glucose into pyruvate. Central nervous system (CNS) pathologies, such as spinal cord injury (SCI) and ischemia, are accompanied by an increase of the glycolytic pathway in the damaged areas as part of the inflammatory response. Pyruvate kinase is a key glycolytic enzyme that converts phosphoenolpyruvate and ADP to pyruvate and ATP. The protein has two isoforms, PKM1 and PKM2, originated from the same gene. As a homodimer, PKM2 loses the pyruvate kinase activity and acts as a transcription factor that regulates the expression of target genes involved in glycolysis and inflammation. After SCI, resident microglia and hematogenous macrophages are key inducers of the inflammatory response with deleterious effects. Activation of the bile acid receptor TGR5 inhibits the pro-inflammatory NFκB pathway in microglia and macrophages. In the present study we have investigated whether bile acids affect the expression of glycolytic enzymes and their regulation by PKM2. Bacterial lipopolysaccharide (LPS) induced the expression of PKM1, PKM2 and its target genes in primary cultures of microglial and Raw264.7 macrophage cells. SCI caused an increase of PKM2 immunoreactivity in macrophages after SCI. Pretreatment with tauroursodeoxycholic acid (TUDCA) or taurolithocholic acid (TLCA) reduced the expression of PKM2 and its target genes in cell cultures. Similarly, after SCI, TUDCA treatment reduced the expression of PKM2 in the lesion center. These results confirm the importance of PKM2 in the inflammatory response in CNS pathologies and indicate a new mechanism of bile acids as regulators of PKM2 pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.