ArticleProgress in neurobiology2025
The low-density lipoprotein receptor-related protein-1 (LRP1) in Schwann cells controls mitochondria homeostasis in peripheral nerves.
Article in Progress in neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Chronic Pain.Brain sciences · 2026Review
- Cell type-specific control of cardiometabolic disease by the dileucine motif of the LDL receptor-related protein LRP1.The Journal of biological chemistry · 2026Article
- Peptide-Incorporated Biomaterials Promote Regeneration of Peripheral Nerve Injuries.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Schwann cell Lrp1 deletion drives trigeminal neuron sensitization and orofacial pain by modulating mitochondrial function and TRPV1/TRPA1 activity.The journal of headache and pain · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Following peripheral nerve injury, Schwann cell (SC) survival is imperative for successful nerve regeneration. The low-density lipoprotein receptor-related protein-1 (LRP1) has been identified as a pro-survival SC plasma membrane signaling receptor, however, the responsible mechanisms underlying SC homeostasis remain incompletely understood. Herein, we establish that LRP1 largely manages mitochondrial dynamics and bioenergetics in SCs by limiting mitochondria fission, maintaining healthy mitochondria membrane potentials, and reducing lactate production associated with peripheral sensitization. When SC LRP1 is suppressed, inner-mitochondria-linked pathways in peripheral nerve proteome are dramatically altered, and cristae integrity in unmyelinated C-fibers is compromised. SC LRP1 protected sensory neurons from mitochondrial dysfunction and modulated mitochondria-related biological pathways in the DRG transcriptome. Conditional deletion of LRP1 in SCs induces pain-related behaviors in mice without nerve injury. Results point to a significant role for LRP1 in SC mitochondrial homeostasis and advance our understanding of the sensory neuron response to alterations in SC bioenergetics.
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Registered trials
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