ArticleMolecular pain
Resilience to capsaicin-induced mitochondrial damage in trigeminal ganglion neurons.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Inhibition of TRPV1 Ameliorates Depression-Like Behaviors in Male Mice by Regulating Neuroinflammation and Neurogenesis via the JAK2/STAT3 Pathway.Molecular neurobiology · 2026Article
- Capsaicin for cardiometabolic syndrome: multitarget mechanisms and therapeutic potential.Frontiers in nutrition · 2026Review
- Capsaicin attenuates sepsis‑associated encephalopathy by inhibiting neuroinflammation and apoptosis whilst activating mitophagy through the BNIP3/NIX pathway.Molecular medicine reports · 2025Article
- TRPV1 channel antagonist capsazepine alleviates morphine tolerance and morphine-induced neurotoxicity by preventing mitochondrial damage and apoptosis: an in vivo and in vitro study.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Associations between dietary intake of mitochondria-related nutrients with the risk of migraine: a prospective study of 202,656 participants.The journal of headache and pain · 2025Article
- Possible Role of Novel Mitochondrial Subsets in Migraine.Life (Basel, Switzerland) · 2025Review
- Obesity-Induced MASLD Is Reversed by Capsaicin via Hepatic TRPV1 Activation.Current issues in molecular biology · 2025Article
- Activation of TRPV1 Channels Inhibits the Release of Acetylcholine and Improves Muscle Contractility in Mice.Cellular and molecular neurobiology · 2023Article
- Energy metabolism disturbance in migraine: From a mitochondrial point of view.Frontiers in physiology · 2023Review
- TRPV1-Mediated Microglial Autophagy Attenuates Alzheimer's Disease-Associated Pathology and Cognitive Decline.Frontiers in pharmacology · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Capsaicin is an agonist of transient receptor potential cation channel subfamily V member 1 (TRPV1). Strong TRPV1 stimulation with capsaicin causes mitochondrial damage in primary sensory neurons. However, the effect of repetitive and moderate exposure to capsaicin on the integrity of neuronal mitochondria remains largely unknown. Our electron microscopic analysis revealed that repetitive stimulation of the facial skin of mice with 10 mM capsaicin induced short-term damage to the mitochondria in small-sized trigeminal ganglion neurons. Further, capsaicin-treated mice exhibited decreased sensitivity to noxious heat stimulation, indicating TRPV1 dysfunction, in parallel with the mitochondrial damage in the trigeminal ganglion neurons. To analyze the capsaicin-induced mitochondrial damage and its relevant cellular events in detail, we performed cell-based assays using TRPV1-expressing PC12 cells. Dose-dependent capsaicin-mediated mitochondrial toxicity was observed. High doses of capsaicin caused rapid destruction of mitochondrial internal structure, while low doses induced mitochondrial swelling. Further, capsaicin induced a dose-dependent loss of mitochondria and autophagy-mediated degradation of mitochondria (mitophagy). Concomitantly, transcriptional upregulation of mitochondrial proteins, cytochrome
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