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Huang, Y.

Publications and source records attributed to Huang, Y..

At least 37 records · Page 2Linked to original sources

DEPICT enables sample-centric therapeutic prioritization across evolving and spatially heterogeneous tumor states

Accurate treatment selection remains a major challenge in precision oncology because tumors with similar genomic alterations can respond differently to therapy. Most drug-response models evaluate individual drugs or drug-sample pairs, whereas clinical decision-making requires therapies to be prioritized within each tumor context. Here we present DEPICT (Drug Efficacy Prediction via Integrated ConText), a sample-centric deep learning framework that reframes drug-response prediction as the relative prioritization of therapies within an individual tumor context. DEPICT integrates transcriptomic and mutational features with prior alteration-therapy relationship and was trained on 231,880 cell line-drug pairs comprising 941 cancer cell lines and 289 compounds. Without retraining, DEPICT retained predictive performance in independently profiled cell lines, experimentally induced drug-resistant states and matched primary lung tumors and patient-derived organoids. Representations learned exclusively from bulk pharmacogenomic data further captured progressive drug-response states at single-cell resolution and outperformed existing single-cell drug-response inference methods. Applied to spatial transcriptomic data, DEPICT resolved clone-associated therapeutic heterogeneity within individual lung tumors, and predicted regional differences were recapitulated in matched multiregional organoid drug-response assays. These findings establish sample-centric therapeutic prioritization as a transferable strategy for modeling dynamic and spatially heterogeneous drug vulnerabilities across biological scales.

bioinformatics↗

Intracranial electrophysiology reveals distinct neural representations of nociception and salience in the human brain

Neuroimaging studies have shown close overlap between neural representations of nociceptive stimuli and non-nociceptive, salient stimuli (such as low-probability sounds), leading to the proposal that nociception and salience share a common neural substrate in the human brain. Here we use high-resolution intracranial recordings from 13 neurosurgical patients (2,018 total electrodes) to show that neural representations of nociception and salience are anatomically and functionally distinct in the human brain. 77% of 107 electrodes that encoded nociceptive stimuli did not encode low-probability sounds ("nociceptive representations"), whereas 23% encoded both nociceptive and low-probability sounds ("salience representations"). Nociceptive representations were distinct from salience representations in terms of anatomical prevalence (posterior insula, inferior parietal, and perirolandic cortex vs. anterior insula, thalamus, and inferior frontal gyrus), timing (nociception preceded salience by 120 ms on a trial-by-trial basis), and function (intracranial electrical stimulation was more likely to cause sensory experience when applied near nociceptive representations, as compared to salience representations). These results provide strong evidence that nociception and salience have distinct neural substrates in the human brain, and that selective measurement of these distinct processes may help understand patient-to-patient variability in chronic pain and develop personalized brain stimulation treatments.

neuroscience↗

A Bispecific Biologic That Robustly Reverses HIV-1 and SIV Latency

Antiretroviral therapy suppresses HIV-1 replication but cannot eliminate the latent viral reservoir persisting in memory CD4 T cells. Existing latency reversal candidates have yet to achieve robust viral reactivation at tolerable doses. We engineered T4IL15{triangleup}, a bispecific biologic that selectively delivers IL-15 signaling to memory CD4 T cells, with minimal off-target stimulation. T4IL15{triangleup} reactivated latent virus in 94% (48/51) of clinical samples ex vivo, 75% (15/20) of administrations in HIV-1-infected and ART-suppressed humanized mice, and 100% (6/6) of SIV-infected and ART-suppressed rhesus macaques at doses well tolerated. We also found that off-target stimulation of non-CD4 cells hindered HIV-1 reactivation ex vivo. T4IL15{triangleup} provides a robust reactivation platform that could complement other reservoir-elimination strategies toward an HIV-1 cure.

microbiology↗

Spatial transcriptomics reveals tumour cell-intrinsic and microenvironmental features associated with survival in high-grade serous ovarian carcinoma

High-grade serous ovarian carcinoma (HGSOC) is the most common form of ovarian carcinoma and accounts for the majority of deaths from the disease, with fewer than half of patients surviving five years after diagnosis. Bulk transcriptomic profiling has identified molecular subtypes and gene-expression signatures associated with shorter or longer survival. However, because bulk profiling measures a composite of tumour and microenvironmental gene expression, the cellular origins of these signatures and their relationship to the tumour microenvironment remain unresolved. To address this, we applied Xenium spatial transcriptomics to treatment-naive HGSOC tumours from 122 patients using a custom 480-gene panel designed to measure tumour-intrinsic gene expression and distinguish immune and stromal cell populations in the surrounding microenvironment. Analysis of tumour-intrinsic gene expression identified 61 genes nominally associated with overall survival, from which Elastic-Net modelling prioritised five genes associated with longer survival and nine associated with shorter survival. Notably, 46 of the 61 associations did not reach the nominal significance threshold when expression was instead aggregated across all cells from the same patients, highlighting how whole-tissue expression can obscure tumour-cell-specific survival associations. Complementary analysis of tumour-proximal cell populations revealed that multiple immune populations were associated with longer survival, whereas two fibroblast populations were associated with shorter survival. Integrating these analyses revealed that survival-associated tumour-intrinsic gene expression was correlated with the abundance of neighbouring immune and stromal populations that were themselves associated with survival. Pairwise Cox regression demonstrated substantial overlap in the prognostic information captured by these features, while analysis of individual gene-cell combinations showed that survival associations differed according to the abundance of neighbouring populations. Consensus clustering further identified four patient groups with distinct combinations of tumour-intrinsic expression and microenvironmental composition, broadly separating patients with longer and shorter survival. Together, this cohort-scale spatial analysis identifies tumour-intrinsic and microenvironmental features associated with HGSOC survival and reveals how their correlated patterns and combined associations relate to patient outcome.

cancer biology↗

Structural streamlining of axonemal doublet microtubules in Plasmodium male gametes

Male gametogenesis in malaria parasites produces up to eight flagellated gametes within approximately 15 min, requiring de novo construction of motile axonemes on an unusually short timescale. Here we combine cellular cryo-electron tomography, high-resolution cryo-EM, proteomics, and parasite genetics to define the molecular architecture and assembly states of the Plasmodium male gamete axoneme. The doublet microtubules retain the principal surface-associated motility modules but contain a markedly reduced luminal microtubule inner protein network. Their inner junction lacks PACRG and is instead organized by CFAP20 and CFAP52, whose combined loss disrupts doublet integrity and exflagellation. We further identify a calmodulin protein at the outer dynein arm docking region and show that outer dynein arms accumulate progressively during gametogenesis. These findings establish distinct form of axonemal remodeling in Plasmodium and reveal the ordered assembly of structural and motor modules during rapid male gamete formation.

cell biology↗

TRIM21 licenses pancreatic acinar fate by modulating BiP phase state through VCP-dependent retrotranslocation

The endoplasmic reticulum (ER) chaperone BiP/GRP78 sits at the center of the proteostasis network, coordinating unfolded protein response (UPR) signaling and supporting oncogenic programs of plasticity, metastasis, immune evasion, and chemoresistance. While BiP undergoes liquid-liquid phase separation in vitro, whether mammalian cells dynamically tune this physicochemical behavior to prevent functional exhaustion or pathological condensation under sustained ER stress has remained unclear. Here, we identify the E3 ubiquitin ligase TRIM21 as a phase-state regulator that suppresses BiP's liquid-to-solid phase separation, clearing, and preventing insoluble aggregates-thereby controlling BiP's localization and availability to sustain the adaptive UPR under ER stress. We found that during ER stress, BiP is prone to liquid-to-solid phase separation, a transition that renders the chaperone dysfunctional. TRIM21 is recruited to BiP, where it directly polyubiquitinates BiP at specific K547/553/554/556 sites with K6-, K27-, K33-, and K63-linked chains; VCP recognizes these marks and extracts BiP from the ER lumen via ER-associated degradation (ERAD), coupling ubiquitin tagging to retrotranslocation. This preserves chaperone availability and sustains adaptive UPR-a homeostatic mechanism broadly relevant to UPR-driven diseases. In vivo, genetic ablation of Trim21 in KrasG12D/+; Pdx1Cre/+ mice triggers aberrant BiP solidification while curtailing acinar-to-ductal transdifferentiation and tumorigenesis; notably, TRIM21 co-localizes with BiP condensates in pre-malignant human pancreatic lesions, underscoring the clinical relevance of this regulatory axis. Our findings define the TRIM21-BiP axis as a phase-control system at the interface of proteostasis and stress adaptation, offering a new framework with translational potential.

cell biology↗

The recoverable resolution of cellular perturbation-response prediction

Virtual cell models aim to predict how cells respond to perturbations, yet accurate prediction of post-perturbation gene expression can conceal failures to recover context-specific responses. Here we identify context geometry compression (CGC), in which models preserve cellular identity and shared perturbation effects while collapsing differences in how the same perturbation acts across contexts. Across biological systems, reproducible context-specific responses remained difficult to recover; in a large drug-response matrix, this persisted even with nearly complete perturbation coverage. The same drug-response predictions achieved higher normalized recovery in predefined pathway summaries than in gene-level response profiles, while coarse response programs were more predictable in human lymphoblastoid cell lines. Compact baseline transcriptomic representations retained most full-RNA predictive performance for patient-specific ex vivo drug responses. Together, these findings establish recoverable biological resolution, rather than measurement dimensionality, as a criterion for evaluating virtual cell predictions and matching model outputs to the biological detail supported by evidence.

bioinformatics↗

Memory-based and surround-based pattern completion show distinct laminar profiles in human V1

Visual input is often incomplete, requiring the brain to infer missing information from prior experience or contextual cues. Establishing whether memory-derived and context-derived information shape pattern completion through shared or distinct top-down pathways is central to understanding how perception emerges from the integration of sensory input and prior knowledge. Across two experiments, we used 7T layer fMRI to measure activity in an occluded region of human V1 while participants viewed natural scenes. Memory-based completion was enabled by varying the level of exposure to full scene images before scanning, while surround-based completion was implemented via two scenes that were repeatedly presented in partially occluded form but never seen intact. In both fMRI experiments, category decoding in the occluded V1 region only emerged after multiple prior exposures, whereas novel scenes did not show reliable decoding. Repeated partially occluded scenes also supported decoding, despite the hidden region never being shown, consistent with surround-based pattern completion. Critically, mnemonic and surround-based pattern completion showed opposite laminar decoding profiles across V1 depths, with mnemonic feedback dominating deep layers, and surround-based feedback dominating superficial layers. Together, these findings suggest that completion in the early visual cortex depends on the sources of inferred information, revealing dissociable feedback pathways for memory- and context-driven inference.

neuroscience↗

Provisional extracellular matrix signaling network regulates tumor lymphoneogenesis and response to immunotherapy

Tertiary lymphoid structures (TLS) predict response to checkpoint inhibition, and conventional dendritic cells (cDC) are required to build and maintain them. What renders a niche permissive for their assembly is unknown: chemokines recruit the cellular constituents but do not specify how they organize. Here we show that the organizing signal is a matrix fragment. Proteolysis of the proteoglycan versican (VCAN) releases the matrikine versikine, constitutively in germinal center light zones and inducibly in tumor stroma. Versikine activates CD11b+ cDC and expands cDC1 to assemble TLS-archetypal triads, apposed DC: CD4+ T: CD8+ T units. Versikine-conditioned DC engage progenitor-exhausted CD8+ T cells (Tpex) and Th1-polarized follicular helper CD4+ T cells. Excess unproteolyzed VCAN inverts this toward DC-Treg crosstalk and Tpex loss. Versikine supplied as mRNA or recombinant protein sensitizes refractory tumors to PD-L1 blockade. VCAN proteolysis prospectively predicted outcomes after PD-1 blockade in metastatic colorectal cancer. Matrikines organize chemokine-recruited cells into functional immune niches.

immunology↗

ctDNA Release Heterogeneity in Luminal Breast Cancer Revealed by Single-Cell Multi-Omics Spatial Analysis

Backgroud Breast cancer is a leading cause of cancer-related mortality, and HR+/HER2-; is the predominant subtype. Molecular pathology, including PIK3CA and ESR1 mutation, informs prognosis and treatment selection. Circulating tumor DNA (ctDNA) offers a non-invasive approach for cancer monitoring, but its clinical utility is limited by tissue plasma discordance, reflecting heterogeneous ctDNA release. The cellular and spatial determinants of this release remain poorly understood, particularly in HR+/HER2-; subtype, where heterogeneity across subclones complicates liquid biopsy interpretation. Results To identify the cellular and spatial determinants of ctDNA release, we developed scMASTER, integrating single-cell transcriptomes and mutations, spatial transcriptomics and matched tumor and plasma DNA sequencing. In ten patients with non-metastatic HR+/HER2- breast cancer, eight recurrent malignant epithelial states showed distinct ctDNA release potential. Antigen-presentation, stress, mitosis and mesenchymal-like states showed high release. PIK3CA and ESR1 mutations were linked to distinct functional states and altered ctDNA detectability. Three spatial architectures, EMT-enriched regions, intraductal luminal progenitors and avascular hypoxic zones, showed high release. Tumor-microenvironment interactions were bidirectional: anti-tumoral immunity correlated with reduced release, whereas immunomodulatory components correlated with increased release. A stratification model based on these features identified high-risk, immunosuppressed patients with poor prognosis, validated across external cohorts. Conclusions Our study establishes a single-cell spatial framework for decoding ctDNA release heterogeneity, linking tumor states, somatic mutations, spatial architecture, and immune interactions to ctDNA release. These findings provide mechanistic insights into tissue-plasma discordance, offer a biological rationale for interpreting ctDNA dynamics, refine patient risk stratification and liquid biopsy-based monitoring in HR+/HER2-; breast cancer.

cancer biology↗

The Dry Truth: Hair-Wetting Improves Dry Electrode EEG Signal Quality

With the rapid advancement of clinical neuroscience and Brain-Computer Interfaces (BCIs), there is an increasing demand for convenient, user-friendly EEG recording methods suitable for diverse environments, including mobile and home-based settings. Traditional gel-based EEG systems, while reliable, are inconvenient and time-consuming, whereas dry electrode systems tend to suffer from elevated noise levels. In this study, we investigated a novel methodological manipulation aimed at enhancing dry electrode signal quality: wetting the hair directly with tap water to improve scalp electrode conductivity. To this end, we recruited 22 healthy participants and compared their resting-state (RS) EEG activity across three experimental conditions (dry, semi-dry, and gel) within a single-session design. Specifically, we analyzed electrode impedance, spectral power (SP), and functional connectivity (FC). Our results show that basic hair-wetting substantially improved mean electrode impedance by 75.7% relative to the dry condition, reduced the proportion of bad channels from approximately 40% to 15%, and increased spectral-power similarity with gel recordings by 7.7% during eyes-closed recordings, and improved FC similarity by approximately 56-70% across frequency bands. Although this method does not fully match the signal quality of traditional gel-based systems, it represents a promising compromise, enhancing EEG data quality under suboptimal conditions. This approach offers a practical and non-invasive means to improve EEG signal quality, ultimately expanding real-world applications of EEG.

neuroscience↗

MetExPred: A Comprehensive Prediction Framework with Protein-Context-Aware Multi-view Learning for Drug Metabolism and Excretion

Within the ADMET continuum, metabolism and excretion (ME) form a critical bridge between drug exposure established by absorption and distribution and downstream efficacy and toxicity. However, no existing framework for drug ME prediction has simultaneously achieved broad coverage of endpoints and robust data recency and completeness. Here, we developed MetExPred, a multi-view prediction framework that comprises 17 classification endpoints and two regression endpoints, covering the overall drug ME process. The framework combines sequence-based and graph-based molecular representations, while optionally incorporating ESM-2 protein representations when experimentally annotated targets are available. A protein-aware masking strategy enables the same architecture to operate in both molecular-only and target-enhanced settings, and multi-view attention adaptively integrates the available representations. Across the classification tasks, MetExPred achieved mean AUROC, AUPRC and F1 scores of 0.844, 0.734 and 0.697, respectively. For clearance and half-life prediction, the model achieved RMSE values of 0.686 and 0.668. MetExPred showed the strongest average performance among the evaluated baselines, while ablation studies confirmed the complementary contributions of molecular sequence, graph and protein information. These results provide a unified and flexible modeling framework for systematic ME prediction of drug compounds, enabling early-stage virtual screening and pharmacokinetic assessment during lead optimization.

bioinformatics↗

White Matter Slow-4 fALFF as a Complementary Marker in the Multimodal Alzheimer's Disease Biomarker Landscape

INTRODUCTION White matter (WM) functional activity, quantified as slow-4 fractional amplitude of low-frequency fluctuations (fALFF; 0.027-0.073 Hz), may reflect Alzheimer's disease (AD) pathology, but its utility relative to established structural imaging markers remains poorly characterized. METHODS We analyzed 369 ADNI-3 participants with baseline resting-state fMRI. Global WM slow-4 fALFF (JHU-20 atlas) was compared against hippocampal volume, entorhinal cortical thickness, FA, and MD across 11 outcomes: plasma biomarkers (pTau217, Abeta42/40, NfL, GFAP; n = 108), PET (amyloid Centiloid, tau SUVR, FDG; n = 66-207), and cognition (MEM, EF, mPACC, MMSE; n = 222-225) using head-to-head benchmarking and variance decomposition. RESULTS WM fALFF was significantly associated with GFAP (partial R2 = 5.35%), amyloid PET (partial R2 = 2.17%), tau PET (partial R2 = 3.52%), executive function (partial R2 = 2.61%), and mPACC (partial R2 = 3.53%). In trimmed models, fALFF explained unique variance in NfL and GFAP beyond FA and MD (unique delta R2: 3.65% and 4.45%), nearly 8-fold greater than DTI's unique contribution for NfL. Gray matter markers showed larger associations with cognition and PET pathology. The incremental value of fALFF was modality-specific: it persisted beyond DTI markers for NfL, GFAP, amyloid PET, executive function, and mPACC, and beyond gray matter markers for NfL and GFAP, but in every domain, including plasma, fALFF was no longer significant when all five imaging markers were entered simultaneously. DISCUSSION WM slow-4 fALFF captures neurodegeneration-related variance, particularly astroglial reactivity and axonal injury, incremental to DTI microstructure and partially independent of gray matter atrophy. These findings position WM functional activity as a complementary, non-invasive imaging marker in the multimodal AD biomarker landscape.

neuroscience↗

Ultra-fast and scalable high-resolution full-length single-cell RNA sequencing using CHART-seq

Plate-based full-length single-cell RNA sequencing resolves transcript structure details but remains difficult to scale because each cell usually requires a separate library. Here we developed CHART-seq (Combinatorial Heteroduplex Assay via Recombinant Tn5), which uses orthogonally indexed Tn5 complexes to tagment RNA/cDNA heteroduplexes and permits early sample pooling. The workflow processed up to 96 cells per library, was compatible with 384-well expansion, and completed library preparation within 3 h at a reagent cost below US$1 per cell. At matched sequencing depth, CHART-seq detected more genes and annotated isoforms than Smart-seq2, Smart-seq3, Flash-seq and SHERRY2, while retaining broad genebody coverage and reproducible expression estimates. In the CHART-seq results of vascular smooth muscle cells, TGF-{beta}1 pretreatment before PDGF-BB exposure partly restored contractile features, suppressed a PDGF-associated inflammatory programme, and induced a distinct metabolic-matrix response with coordinated transcript-usage changes. These biological findings remain exploratory because independent biological replicates were unavailable. CHART-seq provides a rapid, scalable route to full-length single-cell transcript profiling with gene-programme and candidate isoform resolution.

genomics↗

Spatial metabolomics links polyamine turnover and vascular lipid remodeling to barley spikelet fate

Local metabolic programs can determine whether developing organs maintain growth, differentiate, or degenerate. However, the spatial establishment of such programs during reproductive development remains poorly understood. In cereal inflorescences, this question is closely tied to grain number because the fate of initiated floral primordia is shaped by the developmental position, metabolic support, genotype, and environmental stress. To understand the metabolic logic underlying floral fate in barley (Hordeum vulgare L.), we mapped the spatial distribution of metabolites across the inflorescence in wild-type Bowman and in hvcmf4, a mutant that undergoes premature apical inflorescence degeneration. Amino acid-, carbohydrate-, and chlorophyll-associated metabolites form clear developmental gradients along the inflorescence axis. These gradients are progressively remodeled during developmental pre-anthesis tip degeneration but are both accelerated and spatially distorted in hvcmf4. Within this broader metabolic landscape, two discrete domains stand out. First, spermidine-associated domains specifically marked reproductive meristems, a pattern corroborated by the meristem-enriched expression of polyamine biosynthetic genes. This polyamine-rich meristem state declined as developmental tip degeneration proceeded and was prematurely lost in hvcmf4, where polyamine metabolism appeared to shift toward oxidative breakdown via the polyamine oxidase pathway. Second, lysophosphatidylcholine accumulated specifically at floral attachment and vascular supply zones. The developmental reduction of this bioactive lysophospholipid-associated domain in the apical regions, and its stronger disruption in hvcmf4, coincided with the reprogramming of lipid-remodeling and auxin transport-associated genes, suggesting impaired coordination of lipid signaling, auxin canalization, and vascular support. Together, our study reveals spatial polyamine and lysophospholipid domains that couple meristem maintenance with vascular support, providing a metabolic framework for the fate of developing cereal inflorescences.

plant biology↗

Single-cell immune repertoire atlas maps coordinated circulating adaptive immune states in inflammatory bowel disease

Single-cell studies have defined immune states in inflammatory bowel disease (IBD), but how adaptive receptor histories organize circulating immunity remains unclear. We generated a single-cell transcriptomic atlas of peripheral blood from 249 participants with Crohn's disease, ulcerative colitis, or non-IBD control status, including 182 with productive TCR and BCR recovery. Expanded TCR clonotypes marked inflammatory-memory and cytotoxic states, while distinct but similar paired TCRs shared inflammatory programs across participants. BCR lineage maturation linked IgA-associated mucosal and plasma B cell programs to somatic mutation and class switching, distinguishing maturation-associated biology from clonal expansion. Helper, regulatory, and cytotoxic T-cell programs covaried with B-cell states, and inferred interactions nominated reciprocal antigen-presentation and helper pathways. Repertoire-based machine learning distinguished diagnosis, inflammation, and contemporaneous six-month treatment-response status. Together, this atlas connects receptor architecture to coordinated systemic immune remodeling, establishes a foundation for repertoire-informed patient stratification, and prioritizes candidate mechanisms of IBD pathogenesis.

immunology↗

Single-cell profiling reveals stromal niche and α5β1 regulation of neutrophil phenotypes in ulcerative colitis

Background and Aims: Fibroblast-neutrophil interactions are implicated in ulcerative colitis (UC) treatment resistance, but whether fibroblasts modify neutrophil inflammatory activity remains unclear. We investigated responses to fibroblast exposure, stromal depletion, and 5{beta}1-directed treatment. Methods: We integrated human and mouse colonic single-cell RNA sequencing (scRNA-seq), spatial protein profiling (CODEX), fibroblast-neutrophil coculture, and dextran sulfate sodium (DSS) mouse colitis with fibroblast activation protein (FAP) ablation or 5{beta}1-directed treatment. Readouts included cellular representation and protein fluorescence via flow cytometry, neutrophil extracellular trap (NET)-associated elastase activity, RNA programs and epithelial responses using scRNA-seq. Results: Inflamed UC tissue contained higher fractions of inflammatory fibroblasts and oncostatin M (OSM)- and CXCR4-associated neutrophils. Inflammatory fibroblasts had higher FAP-5{beta}1 module scores, and proximity to FAP-high fibroblasts was associated with higher neutrophil OSM and CXCR4 fluorescence. UC fibroblasts increased neutrophil OSM, CXCR4 and myeloperoxidase (MPO) fluorescence and NET-associated elastase activity relative to control fibroblasts, while 5{beta}1-directed treatment attenuated these responses. Both mouse FAP ablation and 5{beta}1 blockade in DSS colitis reduced histologic inflammation and overall neutrophil frequency. Ablation broadly reduced recovered neutrophil representation, whereas blockade increased OSM-positive and PADI4-positive percentages within neutrophils despite lower MPO fluorescence within these subsets. Both interventions were associated with lower epithelial chemokine scores but distinct absorptive and mucus/secretory responses. Conclusions: Fibroblast exposure modifies neutrophil inflammatory phenotype and effector-associated activity, identifying candidate therapeutic pathways in UC. Evaluating these responses alongside neutrophil representation and tissue inflammation could inform pharmacodynamic assessment of stromal-directed therapies.

immunology↗

Spatiotemporal atlas resolves the mesenchymal-epithelial stem cell axis governing human hair follicle aging and pathology

How adult stem cell populations coordinate tissue regeneration across physiological and pathological states remains unclear. Hair follicles contain epithelial and mesenchymal stem cells that codetermine hair regeneration. Here, we integrate a multimodal spatiotemporal atlas with functional validation to define the mesenchymal-epithelial stem cell dynamics governing human hair follicle homeostasis, aging, and androgenetic alopecia. Aging is characterized by passive depletion of hDSC-derived regenerative cues, whereas AGA involves a shift of hDSC toward an inhibitory signaling hub that promotes HFSC dysfunction. We further pinpoint hDSC-secreted PTN as a key regenerative factor that promotes hair growth and counteracts androgen-induced growth suppression. This study provides a holistic framework of adult stem cell crosstalk across physiological and pathological states, offering a mechanistic roadmap to reinstate tissue regeneration.

cell biology↗