ArticleCell reports. Medicine2023
Inflammation-induced mitochondrial and metabolic disturbances in sensory neurons control the switch from acute to chronic pain.
Article in Cell reports. Medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 41 citations in OpenAlex.
- Peripheral nerve injury alters metabolic function and neuronal excitability through the Lin28/let-7 pathway.Science advances · 2026Article
- Wavelength dependent effects of red and infrared photobiomodulation on neuropathic pain, skeletal muscle integrity, and mitochondrial respiration.Lasers in medical science · 2026Article
- Mitochondrial remodeling by extracellular vesicles co-delivering functional mitochondria and a mitophagy inducer for neuropathic pain relief.Materials today. Bio · 2026Article
- Beyond Pain: A Pilot Study of Neurodegenerative and Mitochondrial Pathway Alterations in Sickle Cell Disease Using Platelet Proteomics.Medical sciences (Basel, Switzerland) · 2026Article
- Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Chronic Pain.Brain sciences · 2026Review
- Complex Contributions of Methylglyoxal to Pain, Axon Degeneration, and Diabetic Peripheral Neuropathy.Journal of neurochemistry · 2026Review
- Article
- Association between intrinsic capacity and chronic lung disease among middle-aged and older adults: evidence from CHARLS and ELSA.BMC public health · 2026Article
- Dermal fibroblast mitochondrial profiles in painful diabetic neuropathy.Diabetologia · 2026Article
- Personalizing treatment of pancreatitis-associated chronic pain: the need for an integrated omics approach.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Human pain transcriptomics: lessons learned so far.Pain reports · 2026Review
- Mitochondrial dysfunction at the intersection of alcohol use disorder and chronic pain.Function (Oxford, England) · 2026Review
- Redox-Related Genetic and Biological Ageing Signals in Rapid Pain Progression of Knee Osteoarthritis: A Hypothesis-Generating Analysis in the Osteoarthritis Initiative.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- MASSAG model: Towards an integrative neuroscience framework linking emotional trauma, pain, and mechanisms of force-based manipulations.Neuroscience and biobehavioral reviews · 2026Review
- Neuroimaging-Guided Insights into the Molecular and Network Mechanisms of Chronic Pain and Neuromodulation.International journal of molecular sciences · 2026Review
- Mitochondrial dysfunction in the spinal cord contributes to peripheral hypersensitivity in a nitroglycerin-induced migraine model.Journal of translational medicine · 2026Article
- Garlic-derived bioactive components in neuropathic pain: molecular mechanisms and therapeutic promise.Frontiers in molecular neuroscience · 2026Review
- Schisandrin B confers multi-organ protection via regulation of mitochondrial homeostasis: mechanistic integration, organ-specific differences, and translational challenges-a review.Frontiers in pharmacology · 2026Review
- Dietary Geranylgeraniol Mitigates Pain-Associated Behaviors via Improving Mitochondrial Function and Colon Integrity and Suppressing Neuroinflammation in Male Diabetic Neuropathy Rats.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pain often persists in patients with an inflammatory disease, even when inflammation has subsided. The molecular mechanisms leading to this failure in pain resolution and the transition to chronic pain are poorly understood. Mitochondrial dysfunction in sensory neurons links to chronic pain, but its role in resolution of inflammatory pain is unclear. Transient inflammation causes neuronal plasticity, called hyperalgesic priming, which impairs resolution of pain induced by a subsequent inflammatory stimulus. We identify that hyperalgesic priming in mice increases the expression of a mitochondrial protein (ATPSc-KMT) and causes mitochondrial and metabolic disturbances in sensory neurons. Inhibition of mitochondrial respiration, knockdown of ATPSCKMT expression, or supplementation of the affected metabolite is sufficient to restore resolution of inflammatory pain and prevents chronic pain development. Thus, inflammation-induced mitochondrial-dependent disturbances in sensory neurons predispose to a failure in resolution of inflammatory pain and development of chronic pain.
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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.