About

Wenqin Luo, M.D., Ph.D., is a Professor of Neuroscience and a Professor of the Institute for Regenerative Medicine at the University of Pennsylvania School of Medicine. He serves as the Director of the Penn High Precision Pain Center within the Department of Neuroscience. His research focuses on the molecular and cellular mechanisms underlying mammalian somatosensation and the architecture of the human peripheral nervous system. Luo's work aims to reveal the molecular and cellular architecture of human somatosensory ganglion neurons, understand changes in pathological pain conditions such as migraine, and dissect the evolutionarily conserved mechanisms using mouse genetic tools. His laboratory employs a combination of molecular, cellular, and genetic techniques, including primary human tissue analysis, RNA sequencing, spatial transcriptomics, and AI-assisted histological and behavioral assays, to advance knowledge in pain, itch, touch, and related sensory processes. Luo has made significant contributions to understanding the neural basis of human somatosensation and developing translational reagents for treating chronic pain and itch conditions.

Research topics

• Biology
• Cancer research
• Neuroscience
• Medicine
• Computational biology

Selected publications

• Machine Learning–Driven Fracture Analysis and Prediction in Tight Sandstone Gas Reservoirs Using Geophysical Well Logging

  Journal of Energy Engineering · 2026-05-17

  article
  PublisherDOI

• Etiological basis for chronic pain genetic variation in brain and dorsal root ganglia cell types

  medRxiv · 2025-07-03 · 1 citations

  preprintOpen access

  ABSTRACT Chronic pain is a complex clinical problem comprising multiple conditions that may share a common genetic profile. Genome-wide association studies (GWAS) have identified many risk loci whose cell-type context remains unclear. Here, we integrated GWAS data on chronic pain ( N = 1,235,695) with single-cell RNA sequencing (scRNA-seq) data from human brain and dorsal root ganglia (hDRG), and single-cell chromatin accessibility data from human brain and mouse dorsal horn. Pain-associated variants were enriched in glutamatergic neurons; mainly in prefrontal cortex, hippocampal CA1-3, and amygdala. In hDRG, the hPEP.TRPV1/A1.2 neuronal subtype showed robust enrichment. Chromatin accessibility analyses revealed variant enrichment in excitatory and inhibitory neocortical neurons in brain and in midventral neurons and oligodendrocyte precursor cells in the mouse dorsal horn. Gene-level heritability in the brain highlighted roles for kinase activity, GABAergic synapses, axon guidance, and neuron projection development. In hDRG, implicated genes related to glutamatergic signaling and neuronal projection. In cervical DRG of patients with acute or chronic pain ( N = 12), scRNA-seq data from neuronal or non-neuronal cells were enriched for chronic pain-associated genes (e.g., EFNB2 , GABBR1 , NCAM1 , SCN11A ). This cell-type-specific genetic architecture of chronic pain across central and peripheral nervous system circuits provides a foundation for targeted translational research.

  PublisherOA PDFDOI

• Cancer-associated adipocytes promote peritoneal metastasis of colorectal signet ring cell carcinoma via FABP4 induction

  Cell Communication and Signaling · 2025-12-08

  articleOpen access

  BACKGROUND: Colorectal signet ring cell carcinoma (SRCC) is a rare and aggressive subtype with a high propensity for peritoneal metastasis, yet the underlying mechanisms remain poorly understood. METHODS: We isolated cancer-associated adipocytes (CAAs) from omental tissue adjacent to SRCC peritoneal metastases and examined their morphological and metabolic features compared to normal adipocytes (NAs). Co-culture systems, patient-derived organoids (PDOs), transcriptomic/metabolomic profiling, and peritoneal metastasis mouse models were employed to assess the functional impact of CAAs. The role of fatty acid binding protein 4 (FABP4) and its regulation via CAA-derived exosomes was also investigated. RESULTS: CAAs exhibited a dedifferentiated phenotype, enhanced free fatty acid secretion, and upregulation of matrix metalloproteinases. Co-culture with CAAs significantly promoted SRCC PDO proliferation, stemness, and peritoneal metastasis, accompanied by a metabolic shift toward fatty acid utilization. Among fatty acid metabolism-related genes, FABP4 was markedly upregulated in peritoneal metastases and associated with poor prognosis. Functional assays confirmed that FABP4 promoted fatty acid oxidation (FAO), stemness, and metastasis in PDOs, while FABP4 knockdown abrogated these effects. Mechanistically, CAA-derived exosomes induced FABP4 expression in PDOs, and inhibition of exosome release reversed the pro-tumorigenic phenotypes. CONCLUSIONS: CAA-derived exosomal signaling promotes SRCC aggressiveness through FABP4-mediated fatty acid metabolic reprogramming, identifying FABP4 as a potential therapeutic target for peritoneal metastasis in colorectal SRCC.

  PublisherDOI

• Segmentation Matters: Cell Segmentation Challenge in Spatial Transcriptomics

  SSRN Electronic Journal · 2025-01-01

  preprintOpen accessSenior author
  PublisherDOI

• Correction: myCAF-derived Exosomal PWAR6 accelerates CRC liver metastasis via altering glutamine availability and NK cell function in the tumor microenvironment

  Journal of Hematology & Oncology · 2025-03-18 · 3 citations

  erratumOpen access
  PublisherOA PDFDOI

• Asymmetric Lateral Habenula Function and Peripheral Neural Mechanisms in Regulating Itch-Evoked Scratching

  SSRN Electronic Journal · 2025-01-01

  preprintOpen accessSenior author
  PublisherDOI

• Circular RMST cooperates with lineage-driving transcription factors to govern neuroendocrine transdifferentiation

  Cancer Cell · 2025-04-17 · 17 citations

  articleOpen access
  PublisherOA PDFDOI

• The cell-type–specific genetic architecture of chronic pain in brain and dorsal root ganglia

  Journal of Clinical Investigation · 2025-10-07 · 1 citations

  articleOpen access

  Chronic pain is a complex clinical problem comprising multiple conditions that may share a common genetic profile. GWAS have identified many risk loci whose cell-type context remains unclear. Here, we integrated GWAS data on chronic pain with single-cell RNA-Seq (scRNA-Seq) data from human brain and dorsal root ganglia (hDRG) and single-cell chromatin accessibility data from human brain and mouse dorsal horn. Pain-associated variants were enriched in glutamatergic neurons, mainly in the prefrontal cortex, hippocampal CA1-3, and amygdala. In hDRG, the hPEP.TRPV1/A1.2 neuronal subtype showed robust enrichment. Chromatin accessibility analyses revealed variant enrichment in excitatory and inhibitory neocortical neurons in the brain and in midventral neurons and oligodendrocyte precursor cells in the mouse dorsal horn. Gene-level heritability in the brain highlighted roles for kinase activity, GABAergic synapses, axon guidance, and neuron projection development. In hDRG, implicated genes were related to glutamatergic signaling and neuronal projection. In cervical DRG of patients with acute versus chronic pain, scRNA-Seq data from neuronal or non-neuronal cells were enriched for chronic pain-associated genes (e.g., EFNB2, GABBR1, NCAM1, SCN11A). This cell-type-specific genetic architecture of chronic pain across central and PNS circuits provides a foundation for targeted translational research.

  PublisherOA PDFDOI

• Corrigendum to “circPHF16 suppresses prostate cancer metastasis via modulating miR-581/RNF128/Wnt/β-catenin pathway” [Cell Signal. 2023 Feb;102n110557]

  Cellular Signalling · 2025-07-18

  erratumOpen access
  PublisherDOI

• A Reference Atlas of the Human Dorsal Root Ganglion

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-11-06 · 14 citations

  preprintOpen access

  Somatosensory perception largely emerges from diverse peripheral sensory neurons whose cell bodies reside in dorsal root ganglia (DRG). Damage or dysfunction of DRG neurons is a major cause of chronic pain and sensory loss. In mice, deep single-cell transcriptomic profiling and genetically defined models have offered important clues into DRG function, but in humans, the cellular and molecular landscape of DRG neurons remains less understood. Here, we constructed a reference cell atlas of the human DRG by profiling transcriptomes of cells and nuclei from 126 donors sampled across cervical, thoracic, and lumbar DRGs. This atlas resolves 22 neuronal subtypes, including known and previously unrecognized subtypes linked to nociception, mechanosensation, thermosensation, and proprioception, as well as 10 types of non-neuronal cells. Cross-species integration, spatial transcriptomics, and microneurography enabled cell-type-specific comparisons of soma size and conduction velocity between species. Human DRG somata are larger across all cell types than their mouse counterparts, and the conduction velocities of human hair follicle innervating A-fibers are faster than in mice, suggesting a functional shift in rapid mechanical detection in humans. This integrated human DRG reference cell atlas provides a resource for exploring new molecular and physiological features of human DRG, which could help identify new strategies for treating chronic pain and other diseases of the peripheral nervous system.

  PublisherOA PDFDOI

Recent grants

• Determine Functions of Mammalian Touch-sensing Neurons in Chronic Pain

  NIH · $4.1M · 2013–2023

• Dissection of a new spinal cord circuit in pain sensation

  NIH · $2.5M · 2016–2021

Frequent coauthors

• Jing Li

  Hainan University

  1560 shared

• Wei Wang

  Taipei Veterans General Hospital

  1476 shared

• Lu Gan

  Huazhong University of Science and Technology

  156 shared

• Yichao Wang

  144 shared

• Renjie Wang

  137 shared

• Li Ye

  Zhejiang University

  125 shared

• Huan Wang

  Stanford University

  120 shared

• Haoran Wang

  Northern Jiangsu People's Hospital

  112 shared

Labs

• Wenqin Luo LabPI

Education

• PhD, Neuroscience

  Johns Hopkins School of Medicine

  2005

• MS, Molecular Biology and Biochemistry

  Chinese Academy of Medical Sciences and Peking Union Medical College

  1999

• MD, Clinic Medicine

  Hunan Medical University

  1996