ArticleExperimental neurology2017
Pioglitazone treatment following spinal cord injury maintains acute mitochondrial integrity and increases chronic tissue sparing and functional recovery.
Article in Experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 40 citations in OpenAlex.
- Proteomics reveal PTEN as a critical mediator of sustained mitochondrial dysfunction during chronic spinal cord injury.Experimental neurology · 2026Article
- Medicinal Chemistry Review of the NEET Protein Family.ChemMedChem · 2026Review
- Curcumin nanocrystals mitigate hypoxia-induced cardiac injury through redox regulation and CHOP-CytC-caspase pathway modulation.Scientific reports · 2026Article
- PPAR-γ activation by pioglitazone inhibits microglia-mediated neuroinflammation and alleviates disease in neuromyelitis optica spectrum disorders.Acta neuropathologica communications · 2025Article
- Pioglitazone Modulates Microglia M1/M2 Polarization Through PPAR-γ Pathway and Exerts Neuroprotective Effects in Experimental Subarachnoid Hemorrhage.Molecular neurobiology · 2025Article
- Loss of the mitochondrial protein mitoNEET in mice is associated with cognitive impairments and increased neuroinflammation.Journal of Alzheimer's disease : JAD · 2025Article
- The Neuroprotective Mechanisms of PPAR-γ: Inhibition of Microglia-Mediated Neuroinflammation and Oxidative Stress in a Neonatal Mouse Model of Hypoxic-Ischemic White Matter Injury.CNS neuroscience & therapeutics · 2024Article
- Drug Repurposing for Spinal Cord Injury: Progress Towards Therapeutic Intervention for Primary Factors and Secondary Complications.Pharmaceutical medicine · 2023Review
- Delivery of mitoceuticals or respiratory competent mitochondria to sites of neurotrauma.Mitochondrion · 2023Review
- Pioglitazone restores mitochondrial function but does not spare cortical tissue following mild brain contusion.Brain communications · 2023Article
- Peroxisome proliferator-activated receptor-γ doesn't modify altered electrophysiological properties of the CA1 pyramidal neurons in a rat model of hepatic cirrhosis.Metabolic brain disease · 2022Article
- PPAR agonists attenuate lenalidomide's anti-myeloma activity in vitro and in vivo.Cancer letters · 2022Article
- Rescuing mitochondria in traumatic brain injury and intracerebral hemorrhages - A potential therapeutic approach.Neurochemistry international · 2021Review
- FDA-approved 5-HTExperimental neurology · 2021Article
- Interplay of Opposing Effects of the WNT/β-Catenin Pathway and PPARγ and Implications for SARS-CoV2 Treatment.Frontiers in immunology · 2021Review
- Mitochondria focused neurotherapeutics for spinal cord injury.Experimental neurology · 2020Review
- Can pioglitazone be potentially useful therapeutically in treating patients with COVID-19?Medical hypotheses · 2020Article
- Bioenergetic restoration and neuroprotection after therapeutic targeting of mitoNEET: New mechanism of pioglitazone following traumatic brain injury.Experimental neurology · 2020Article
- Nanoparticle formulation and in vitro efficacy testing of the mitoNEET ligand NL-1 for drug delivery in a brain endothelial model of ischemic reperfusion-injury.International journal of pharmaceutics · 2020Article
- Rational Design, Synthesis, and In Vitro Neuroprotective Evaluation of Novel Glitazones for PGC-1α Activation via PPAR-γ: a New Therapeutic Strategy for Neurodegenerative Disorders.Neurotoxicity research · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Pioglitazone is an FDA-approved PPAR-γ agonist drug used to treat diabetes, and it has demonstrated neuroprotective effects in multiple models of central nervous system (CNS) injury. Acute treatment after spinal cord injury (SCI) in rats is reported to suppress neuroinflammation, rescue injured tissues, and improve locomotor recovery. In the current study, we additionally assessed the protective efficacy of pioglitazone treatment on acute mitochondrial respiration, as well as functional and anatomical recovery after contusion SCI in adult male C57BL/6 mice. Mice received either vehicle or pioglitazone (10mg/kg) at either 15min or 3h after injury (75kdyn at T9) followed by a booster at 24h post-injury. At 25h, mitochondria were isolated from spinal cord segments centered on the injury epicenters and assessed for their respiratory capacity. Results showed significantly compromised mitochondrial respiration 25h following SCI, but pioglitazone treatment that was initiated either at 15min or 3h post-injury significantly maintained mitochondrial respiration rates near sham levels. A second cohort of injured mice received pioglitazone at 15min post injury, then once a day for 5days post-injury to assess locomotor recovery and tissue sparing over 4weeks. Compared to vehicle, pioglitazone treatment resulted in significantly greater recovery of hind-limb function over time, as determined by serial locomotor BMS assessments and both terminal BMS subscores and gridwalk performance. Such improvements correlated with significantly increased grey and white matter tissue sparing, although pioglitazone treatment did not abrogate long-term injury-induced inflammatory microglia/macrophage responses. In sum, pioglitazone significantly increased functional neuroprotection that was associated with remarkable maintenance of acute mitochondrial bioenergetics after traumatic SCI. This sets the stage for dose-response and delayed administration studies to maximize pioglitazone's efficacy for SCI while elucidating the precise role that mitochondria play in governing its neuroprotection; the ultimate goal to develop novel therapeutics that specifically target mitochondrial dysfunction.
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