ArticlePain2026
Piezo2 mediates mechanical sensitivity and injury-induced hypersensitivity in MrgprD-expressing nociceptors.
Article in Pain, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Cold-gated potentiation of mechanotransduction supports touch sensation below 5°C in a mammalian hibernator.Current biology : CB · 2026Article
- A dual role of PIEZO2 in neuropathic pain: driving peripheral sensitization and enabling mechanical loading-induced analgesia.Cell communication and signaling : CCS · 2026Article
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Authors and funding
5 authors.
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Abstract
abstractPiezo2 is a mechanotransducer essential for detecting low-threshold tactile and proprioceptive stimuli. Emerging evidence suggests its involvement in pain sensing, particularly in mechanical allodynia. Transcriptomic data revealed high Piezo2 expression in MrgprD-expressing neurons, a population of nonpeptidergic nociceptors implicated in physiological and pathological mechanical pain. However, the specific function of Piezo2 in these pain-sensing neurons and its potential contribution to mechanical hyperalgesia induced by nerve injury remains unclear. We used in vitro calcium imaging to functionally characterize MrgprD + neurons in adult mouse dorsal root ganglia (DRG) and performed whole-cell mechano patch-clamp recordings to characterize their mechanosensitivity. Approximately half of MrgprD + neurons displayed mechanically activated currents. These currents were abolished in MrgprD + DRG neurons from conditional knockout mice lacking Piezo2 specifically in this population. Behavioral experiments using the sciatic nerve chronic constriction injury mouse model revealed reduced mechanical hypersensitivity to high-intensity stimuli in mice lacking Piezo2 specifically in MrgprD + neurons. In vivo calcium imaging of lumbar DRG showed increased activity of MrgprD + neurons in response to noxious mechanical stimulation of the hind paw under chronic constriction injury-induced neuropathic pain. Conditional deletion of Piezo2 abolished this sensitization and significantly decreased the proportion of MrgprD + neurons responsive to mechanical stimuli. Collectively, these findings highlight Piezo2 as a key mediator of noxious mechanical sensitivity in MrgprD + neurons under both physiological and neuropathic pain conditions.
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