ArticleMolecular neurobiology2024
Intranasal Delivery of Mitochondria Attenuates Brain Injury by AMPK and SIRT1/PGC-1α Pathways in a Murine Model of Photothrombotic Stroke.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 24 citations in OpenAlex.
- Intercellular Mitochondrial Transfer in the Nervous System: Roles of Tunneling Nanotubes, Mitochondrial Extracellular Vesicles, and Neuroimmune Bioenergetic Interactions.Molecular neurobiology · 2026Review
- SIRT1/AMPK/PGC1α pathway in ischemic stroke: Elucidating neuroprotective strategies (Review).Molecular medicine reports · 2026Review
- Activation of sarco/endoplasmic reticulum Ca²⁺-ATPase 2 (SERCA2) reduces brain injury and improves cognitive function following ischemic stroke.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Intercellular Mitochondrial Transfer as Endogenous Neuroprotection: Mechanisms and Therapeutic Implications in Ischemic Stroke.Translational stroke research · 2026Review
- Exercise Improves Mitochondrial Homeostasis: A Potential Neuroprotective Strategy for Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2026Review
- Cerebral Ischemia-Reperfusion Injury: Unraveling the Mitophagy-Oxidative Stress Axis for Neuroprotective Strategies.International journal of molecular sciences · 2026Review
- Mitochondrial Transplantation Therapy for Ischemic Stroke: Progress and Challenges.Cellular and molecular neurobiology · 2026Review
- Mitochondrial Transplantation as a Therapeutic Strategy for Inherited Mitochondrial Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Recent Advances in Mitochondrial Transplantation for Ischemic Stroke: A Review of in Vitro and in Vivo Studies.Translational stroke research · 2026Review
- Additive protection of transcranial direct current stimulation and mitochondrial transplantation on ischemic stroke via inducing A2 astrocytes.Frontiers in molecular neuroscience · 2026Article
- Therapeutic transplantation of mitochondria and Extracellular Vesicles: Mechanistic insights into mitochondria bioenergetics, redox signaling, and organelle dynamics in preclinical models.Free radical biology & medicine · 2025Review
- Intranasal Drug Delivery Technology in the Treatment of Central Nervous System Diseases: Challenges, Advances, and Future Research Directions.Pharmaceutics · 2025Review
- The Nasal-Brain Drug Delivery Route: Mechanisms and Applications to Central Nervous System Diseases.MedComm · 2025Review
- Dual Action ofNutrients · 2025Article
- SIRT1 and miR-34a as Potential Plasma Biomarkers in the Acute Phase of Ischemic Stroke.International journal of molecular and cellular medicine · 2025Article
- The critical role of Sirt1 in ischemic stroke.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Ischemic stroke is one of the major causes of morbidity and mortality worldwide. Mitochondria play a vital role in the pathological processes of cerebral ischemic injury, but its transplantation and underlying mechanisms remain unclear. In the present study, we examined the effects of mitochondrial therapy on the modulation of AMPK and SIRT1/PGC-1α signaling pathway, oxidative stress, and NLRP3 inflammasome activation after photothrombotic ischemic stroke (pt-MCAO). The adult male mice were subjected to the pt-MCAO in which the proximal-middle cerebral artery was exposed with a 532-nm laser beam for 4 min by retro-orbital injection of a photosensitive dye (Rose Bengal: 15 mg/kg) before the laser light exposure and isolated mitochondria (100 μg protein) were administered intranasally at 30 min, 24 h, and 48 h following post-stroke. After 72 h, mice were tested for neurobehavioral outcomes and euthanized for infarct volume, brain edema, and molecular analysis. First, we found that mitochondria therapy significantly decreased brain infarct volume and brain edema, improved neurological dysfunction, attenuated ischemic stroke-induced oxidative stress, and neuroinflammation. Second, mitochondria treatment inhibited NLRP3 inflammasome activation. Finally, mitochondria therapy accelerated p-AMPKα(Thr172) and PGC-1α expression and resorted SIRT1 protein expression levels in pt-MCAO mice. In conclusion, our results demonstrate that mitochondria therapy exerts neuroprotective effects by inhibiting oxidative damage and inflammation, mainly dependent on the heightening activation of the AMPK and SIRT1/PGC-1α signaling pathway. Thus, intranasal delivery of mitochondria might be considered a new therapeutic strategy for ischemic stroke treatment.
Indexed as
Identifiers
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.