ReviewFree radical biology & medicine2016
PPARγ as a therapeutic target to rescue mitochondrial function in neurological disease.
Review in Free radical biology & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
169 citing papers in PubMed, 253 citations in OpenAlex.
- Trial
- PPARγ Signaling in the Central Nervous System: A Review of the Implications in Synaptic Plasticity, Neuroinflammatory and Neoplastic Processes.Neurochemical research · 2026Review
- ADSC-derived mitochondrial nanovesicles transplantation alleviates capsular fibrosis and inflammation and improves joint mobility in a rat model of adhesive capsulitis.Journal of orthopaedic translation · 2026Article
- Stephanoside B modulates metabolic gene expression and lengthens the circadian bmal1 oscillation period in differentiated myotubes revealed by real-time bioluminescence.Molecular biology reports · 2026Article
- Comparative Study of Young and MaturePlants (Basel, Switzerland) · 2026Article
- Neurodegenerative NMNAT2 Deficiency Promotes APP Processing in a SARM1-Dependent Manner.Cells · 2026Article
- Pioglitazone protects against trimethyltin hippocampal injury by reducing pyroptosis, mitochondrial dysregulation and ER stress.Scientific reports · 2026Article
- Metabolic adaptation to IMMT deficiency through the ATF6-PPARγ axis is contingent on TP53 mutation status in breast cancer.Cell death & disease · 2026Article
- Predifferentiation Neurotoxicity of GenX Exposure on hiPSC-Derived Cortical Neurons.Environmental science & technology · 2026Article
- Serum-Derived Extracellular Vesicles as Biological Indicator of Mobility Resilience in Older Adults.Aging cell · 2026Article
- Caspase-6 Controls Lipid and Energy Metabolism in Diet-Induced Obesity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Butyrate extends health and lifespan in mice with mitochondrial deficiency.Nature communications · 2026Article
- Developmental programming: gestational exposure to excess testosterone disrupts maternal steroid homeostasis and perturbs the steroid-lipid relationship in sheep.Molecular and cellular endocrinology · 2026Article
- The GPR124‑Wnt‑PPARγ regulatory axis: Molecular mechanisms and therapeutic implications in chronic inflammatory diseases (Review).International journal of molecular medicine · 2026Review
- Article
- Glycosylation Matters: Network Pharmacology-Based and Molecular Docking Analysis of Resveratrol Glycosylated Derivatives on Parkinson's Disease.ACS omega · 2026Article
- Butyrate extends health and lifespan in mice with mitochondrial deficiency.bioRxiv : the preprint server for biology · 2026Article
- Cyasterone Improves Mitochondrial Function and Protects against Knee Osteoarthritis by Activating PPARγ.Current medicinal chemistry · 2026Article
- Microglia Polarization: A Key Regulatory Mechanism of Neuropathic Pain.Journal of pain research · 2026Review
- Andrographolide Attenuates Sepsis-Induced Acute Lung InjuryEndocrine, metabolic & immune disorders drug targets · 2026Article
109 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
There is increasing evidence for the involvement of mitochondrial dysfunction and oxidative stress in the pathogenesis of many of the major neurodegenerative and neuroinflammatory diseases, suggesting that mitochondrial and antioxidant pathways may represent potential novel therapeutic targets. Recent years have seen a rapidly growing interest in the use of therapeutic strategies that can limit the defects in, or even to restore, mitochondrial function while reducing free radical generation. The peroxisome proliferation-activated receptor gamma (PPARγ), a ligand-activated transcription factor, has a wide spectrum of biological functions, regulating mitochondrial function, mitochondrial turnover, energy metabolism, antioxidant defence and redox balance, immune responses and fatty acid oxidation. In this review, we explore the evidence for potential beneficial effects of PPARγ agonists in a number of neurological disorders, including Parkinson's disease, Alzheimer's disease, Amyotrophic lateral sclerosis and Huntington's disease, ischaemia, autoimmune encephalomyelitis and neuropathic pain. We discuss the mechanisms underlying those beneficial effects in particular in relation to mitochondrial function, antioxidant defence, cell death and inflammation, and suggest that the PPARγ agonists show significant promise as therapeutic agents in otherwise intractable neurological disease.
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What OpenQuestion holds
Registered trials
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.