ArticleRedox biology2022
Adiponectin/AdiopR1 signaling prevents mitochondrial dysfunction and oxidative injury after traumatic brain injury in a SIRT3 dependent manner.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 100 citations in OpenAlex.
- Targeted blood-brain barrier penetration for traumatic brain injury therapy via RXR/PPAR-driven microglial M2 polarization.Materials today. Bio · 2026Article
- Fumarate Hydratase Lactylation Exacerbates Traumatic Brain Injury Pathology via Mitochondrial Dysfunction and Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ultrasound-Responsive Piezoelectric Fibrous Membrane Promotes Neurological Recovery After TBI by Modulating Microglial Polarization via Restoring Mitochondrial Dynamic Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanism of action of synaptic mitochondrial damage in delayed cognitive recovery.Neural regeneration research · 2026Article
- The AMPK-BECN1-System Xc⁻ Pathway in Traumatic Brain Injury: Implications for Exosome-Based Therapy.Cellular and molecular neurobiology · 2026Review
- Red Blood Cell-Derived Exosomes Deliver Complement C5 to Exacerbate Neuroinflammation and Neuronal Injury after Intracerebral Hemorrhage.Inflammation · 2026Article
- Adiponectin Inhibits Oxidative Stress and Tight Junction Protein Loss: Evidence from a Hepatic Encephalopathy Mouse Model and Brain Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Amantadine Attenuates Secondary Oxidative and Inflammatory Injury by Modulating the HIF-1α/BNIP3L/HMGB1 Axis in Rat Model of Traumatic Brain Injury.Medicina (Kaunas, Lithuania) · 2026Article
- Circulating adipokines level and the risk of neurodegenerative diseases: a two‑sample mendelian randomization study and proteomic analysis.BMC neurology · 2026Article
- Zipper-interacting Protein Kinase Modulates Gene Expression Linked to Synaptic and Neuronal Processes after Traumatic Brain Injury.Molecular neurobiology · 2026Article
- Targeting mitofusin 1-mediated mitochondrial dynamics to suppress neuroinflammation and pyroptosis after traumatic brain injury.Burns & trauma · 2026Article
- Irisin may be involved in exendin-4 mitochondrial action in human adipocytes.Archives of medical science : AMS · 2026Article
- Kynurenine Pathway Metabolites as Mediators of Exercise-Induced Mood Enhancement, Fatigue Resistance, and Neuroprotection.International journal of molecular sciences · 2025Review
- Sirtuin 3 in diabetic kidney disease: mechanisms and pharmacotherapy.Renal failure · 2025Review
- Summarizing the Role of Selected Adipokines in Parkinson's Disease: What Is Known About Leptin, Adiponectin, Resistin, Visfatin, and Progranulin in Neurodegeneration?Molecules (Basel, Switzerland) · 2025Review
- Mulberrin Alleviates Renal Ischemia-Reperfusion by Inhibiting Ferroptosis and Oxidative Stress Through Sirt3 Activation.Biomedicines · 2025Article
- FGF21 maintains redox homeostasis and promotes neuronal survival after traumatic brain injury by targeting SLC25A39-mediated mitochondrial GSH transport.Journal of translational medicine · 2025Article
- Rebuilding Mitochondrial Homeostasis and Inhibiting Ferroptosis: Therapeutic Mechanisms and Prospects for Spinal Cord Injury.Biomedicines · 2025Review
- Strengthening monocarboxylate transporters by adiponectin receptor agonist ameliorates diabetic peripheral neuropathy.Cell communication and signaling : CCS · 2025Article
- Pharmacological Blocking of Adiponectin Receptors Induces Alzheimer's Disease-like Neuropathology and Impairs Hippocampal Function.Biomedicines · 2025Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction and oxidative injury, which contribute to worsening of neurological deficits and poor clinical outcomes, are hallmarks of secondary brain injury after TBI. Adiponectin (APN), beyond its well-established regulatory effects on metabolism, is also essential for maintaining normal brain functions by binding APN receptors that are ubiquitously expressed in the brain. Currently, the significance of the APN/APN receptor (AdipoR) signaling pathway in secondary injury after TBI and the specific mechanisms have not been conclusively determined. In this study, we found that APN knockout aggravated brain functional deficits, increased brain edema and lesion volume, and exacerbated oxidative stress as well as apoptosis after TBI. These effects were significantly alleviated after APN receptor agonist (AdipoRon) treatment. Moreover, we found that AdipoR1, rather than AdipoR2, mediated the protective effects of APN/AdipoR signaling against oxidative stress and brain injury after TBI. In neuron-specific AdipoR1 knockout mice, mitochondrial damage was more severe after TBI, indicating a potential association between APN/AdipoR1 signaling inactivation and mitochondrial damage. Mechanistically, neuron-specific knockout of SIRT3, the most important deacetylase in the mitochondria, reversed the neuroprotective effects of AdipoRon after TBI. Then, PRDX3, a critical antioxidant enzyme in the mitochondria, was identified as a vital downstream target of the APN/SIRT3 axis to alleviate oxidative injury after TBI. Finally, we revealed that APN/AdipoR1 signaling promotes SIRT3 transcription by activating the AMPK-PGC pathway. In conclusion, APN/AdipoR1 signaling plays a protective role in post-TBI oxidative damage by restoring the SIRT3-mediated mitochondrial homeostasis and antioxidant system.
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