American Journal of Pathology最新文献

{"title":"Microglia Promote Neurodegeneration and Hyperkatifeia during Withdrawal and Abstinence from Binge Alcohol","authors":"Elizabeth M. McNair ,&nbsp;Lamar W. Dawkins ,&nbsp;Baylee Materia ,&nbsp;Grace Ross ,&nbsp;Alexandra Barnett ,&nbsp;Puja Nakkala ,&nbsp;Liya Qin ,&nbsp;Jian Zou ,&nbsp;Viktoriya Nikolova ,&nbsp;Sheryl Moy ,&nbsp;Leon G. Coleman Jr.","doi":"10.1016/j.ajpath.2025.10.005","DOIUrl":"10.1016/j.ajpath.2025.10.005","url":null,"abstract":"<div><div>Proinflammatory microglial polarization, neuronal death, and hyperkatifeia/negative affect during withdrawal are key features of alcohol use disorder (AUD). However, the role microglia play in the development of AUD-related neuronal and behavioral pathology is unclear. Given the ability of microglia to impact neuronal function, it was hypothesized that proinflammatory microglia promote neuronal death and hyperkatifeia during prolonged abstinence from binge alcohol. Proinflammatory signaling and affective state were assessed in mice either during acute withdrawal (24 hours) or abstinence (&gt;4 weeks) to binge alcohol exposure. Ten days of binge alcohol increased proinflammatory gene signaling 24 hours after ethanol, which lasted weeks into withdrawal. Alcohol reduced brain-derived neurotrophic factor in hyperkatifeia-associated regions (ie, the central amygdala and infralimbic cortex) during acute withdrawal and caused persistent microglial structural changes and loss of microglial brain-derived neurotrophic factor in the bed nucleus of the stria terminalis during abstinence. This was associated with increased anxiety-like behavior and hyperarousal, with persistent enhancement of conditioned fear memory during abstinence. Inhibition of proinflammatory microglia with Gi designer receptors exclusively activated by designer drugs blocked neuronal death and prevented persistent proinflammatory gene induction and hyperkatifeia in female mice. Thus, this identifies a direct role for microglia in the development of AUD-related neuropathology and behavioral dysfunction, implicating microglia as cellular targets for the prevention of AUD phenotypes.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"196 1","pages":"Pages 306-325"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145429953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Update on IL-22 Therapies in Alcohol-Associated Liver Disease and Beyond","authors":"Lihong Fu ,&nbsp;Burhan Yokus ,&nbsp;Bin Gao ,&nbsp;Pal Pacher","doi":"10.1016/j.ajpath.2025.03.010","DOIUrl":"10.1016/j.ajpath.2025.03.010","url":null,"abstract":"<div><div>Excessive alcohol consumption drives the development of alcohol-associated liver disease (ALD), including steatohepatitis, cirrhosis, and hepatocellular carcinoma, and its associated complications, such as hepatorenal syndrome. Hepatocyte death, inflammation, and impaired liver regeneration are key processes implicated in the pathogenesis and progression of ALD. Despite extensive research, therapeutic options for ALD remain limited. IL-22 has emerged as a promising therapeutic target because of its hepatoprotective properties mediated through the activation of the STAT3 signaling pathway. IL-22 enhances hepatocyte survival by mitigating apoptosis, oxidative stress, and inflammation while simultaneously promoting liver regeneration through the proliferation of hepatocytes and hepatic progenitor cells and the up-regulation of growth factors. Additionally, IL-22 exerts protective effects on epithelial cells in various organs affected by ALD and its associated complications. Studies from preclinical models and early-phase clinical trials of IL-22 agonists, such as F-652 and UTTR1147A, have shown favorable safety profiles, good tolerability, and encouraging efficacy in reducing liver injury and promoting regeneration. However, the heterogeneity and multifactorial nature of ALD present ongoing challenges. Further research is needed to optimize IL-22–based therapies and clarify their roles within a comprehensive approach to ALD management. This review summarizes the current understanding of IL-22 biology and its role in ALD pathophysiology and ALD-associated complications along with therapeutic application of IL-22, potential benefits, and limitations.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"196 1","pages":"Pages 136-150"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transforming Growth Factor-β Signaling in Alcohol-Associated Liver Disease","authors":"Huihui Zou ,&nbsp;Sai Wang ,&nbsp;Chenjun Huang ,&nbsp;Steven Dooley ,&nbsp;Nadja M. Meindl-Beinker","doi":"10.1016/j.ajpath.2025.09.017","DOIUrl":"10.1016/j.ajpath.2025.09.017","url":null,"abstract":"<div><div>Transforming growth factor-β (TGF-β) signaling exerts broad regulatory effects on alcohol-associated liver disease (ALD) progression, influencing processes such as hepatocellular injury, regeneration, inflammation, fibrogenesis, cirrhosis, carcinogenesis, and hepatic failure. TGF-β modifies alcohol-induced signals in multiple liver-resident cell types, including hepatocytes, hepatic stellate cells, liver sinusoidal endothelial cells, and immune populations, particularly macrophages. To delineate its context-specific roles in ALD, 154 of 421 PubMed-listed publications (2000 to 2025; search terms TGF-β and alcohol and liver disease) were reviewed, supplemented by 19 foundational studies published earlier. In hepatocytes, TGF-β promotes oxidative stress, apoptosis, metabolic reprogramming, and epithelial-to-mesenchymal transition. In hepatic stellate cells and Kupffer cells, gut-derived endotoxins, ethanol, and unsaturated fatty acids induce TGF-β alongside proinflammatory cytokines. Ethanol metabolism generates acetaldehyde, which drives TGF-β and receptor expression, enhances canonical and noncanonical signaling, and engages epigenetic regulators to promote extracellular matrix deposition. In liver sinusoidal endothelial cells, alcohol-induced TGF-β suppresses proliferation, contributing to sinusoidal capillarization, impaired endothelial regeneration, and fibrogenesis. TGF-β dampens clearance of damaged hepatocytes and perpetuating chronic injury by suppressing natural killer cell cytotoxicity and promoting regulatory T-cell differentiation. At end-stage disease, TGF-β promotes expansion and fate switching of cholangiocyte-derived liver progenitor cells to replenish lost hepatocytes. Despite its central role in ALD, therapeutic exploitation of TGF-β signaling remains underexplored. Future studies should define cell type–specific signaling nodes to enable precision therapies.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"196 1","pages":"Pages 50-67"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Seminal Work That Defined the Pathology of Frontotemporal Dementias and the Concept of TDP-43 Proteinopathies","authors":"Steven L. Carroll","doi":"10.1016/j.ajpath.2025.09.004","DOIUrl":"10.1016/j.ajpath.2025.09.004","url":null,"abstract":"","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 12","pages":"Pages 2251-2253"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145555193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low Potassium Triggers Tubular Epithelial NLR Family Pyrin Domain-Containing 3/Apoptosis-Associated Speck-Like Protein-Containing a CARD–Driven Kidney Inflammation Independently of Inflammasomes","authors":"Satoko Komori ,&nbsp;Takanori Komada ,&nbsp;Takayoshi Matsumura ,&nbsp;Tadayoshi Karasawa ,&nbsp;Yutaka Miura ,&nbsp;Chintogtokh Baatarjav ,&nbsp;Yoshitaka Gunji ,&nbsp;Hidetoshi Aizawa ,&nbsp;Yoshiko Mizushina ,&nbsp;Noriyoshi Fukushima ,&nbsp;Toru Sugihara ,&nbsp;Satoshi Ando ,&nbsp;Tetsuya Fujimura ,&nbsp;Daisuke Nagata ,&nbsp;Masafumi Takahashi","doi":"10.1016/j.ajpath.2025.08.010","DOIUrl":"10.1016/j.ajpath.2025.08.010","url":null,"abstract":"<div><div>Pathologic potassium (K⁺) deficiency causes kidney inflammation and injury, known as hypokalemic nephropathy (HN), the underlying pathogenesis of which is obscure. NLR family pyrin domain-containing 3 (NLRP3) inflammasomes are platforms that sense the reduction of intracellular K⁺, engaging inflammation and tissue injury. The present study investigated whether or not systemic K⁺ deficiency induces NLRP3 inflammasome activation in HN. Clinically diagnosed HN in humans manifested up-regulation of NLRP3 and apoptosis-associated speck-like protein-containing a CARD (ASC) in the kidney epithelia. A K⁺ depletion model in mice demonstrated that kidney-resident NLRP3 and ASC play key roles in triggering early inflammation in HN kidneys. Unexpectedly, the K⁺ depletion-induced kidney inflammation was not dependent on inflammasome activation. A single-cell RNA-sequencing analysis revealed ASC up-regulation, NF-κB activation, and an increased level of tumor necrosis factor–like weak inducer of apoptosis receptor fibroblast growth factor-inducible 14 (FN14) in the HN kidneys, primarily in the distal nephron/collecting duct epithelial cells. Although kidney epithelial cells did not drive NLRP3 inflammasomes, NLRP3 and ASC alternatively enhanced with-no-lysine kinase-dependent NF-κB signaling in response to tumor necrosis factor–like weak inducer of apoptosis under a low-K⁺ milieu. These findings indicate a unique proinflammatory cascade mediated by NLRP3 and ASC beyond the framework of inflammasomes, which broadens the understanding of electrolyte-associated immunity in the kidney.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 12","pages":"Pages 2336-2355"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stromal Steroid 5 Alpha-Reductase 2 Promotes Prostate Growth through WNT5A–Lymphoid Enhancer–Binding Factor 1–Insulin-Like Growth Factor 1 Signaling in Benign Prostatic Hyperplasia","authors":"Christina Sharkey ,&nbsp;Boqing Gu ,&nbsp;Xingbo Long ,&nbsp;Yao Tang ,&nbsp;Nicolas Patsatzis ,&nbsp;Steven Li ,&nbsp;Aria F. Olumi ,&nbsp;Zongwei Wang","doi":"10.1016/j.ajpath.2025.08.011","DOIUrl":"10.1016/j.ajpath.2025.08.011","url":null,"abstract":"<div><div>Steroid 5 α-reductase 2 (SRD5A2) is a key enzyme in androgen metabolism and a pharmacologic target in benign prostatic hyperplasia. Although SRD5A2 is known to mediate stromal-epithelial interactions that influence prostate growth, the relationship between baseline SRD5A2 expression and prostate volume remains unclear. In this study, SRD5A2 expression was analyzed in human prostate tissues from the Medical Therapy of Prostatic Symptoms trial and institutional biorepository cohorts. Quantitative assessments were performed and correlations were evaluated between expression level of SRD5A2, WNT5A, prostate volume, and tissue signaling profiles. SRD5A2 expression was significantly associated with total prostate and transition zone volume. Stromal-specific WNT5A expression showed a strong positive correlation with SRD5A2, whereas neither serum nor tissue dihydrotestosterone levels correlated with SRD5A2 expression. In <em>Srd5a2-</em>null mice, Wnt5a expression in the prostate stroma was dependent on Srd5a2 and showed region-specific regulation. Mechanistically, SRD5A2 overexpression in human prostate stromal cells up-regulated WNT5A and lymphoid enhancer–binding factor 1, activated insulin-like growth factor 1 (IGF1) signaling, increased proliferation, and reduced apoptosis. Conditioned media from these cells enhanced epithelial proliferation through paracrine IGF1 activity. This study provides the first evidence that SRD5A2 promotes prostate growth through a stromal WNT5A–lymphoid enhancer–binding factor 1–IGF1 paracrine signaling axis independent of androgen levels, suggesting a novel therapeutic mechanism relevant for patients with benign prostatic hyperplasia with resistance to conventional 5 α-reductase inhibitor therapy.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 12","pages":"Pages 2411-2430"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Gut Microbiome as a Possible Mediator in Autoimmunity and Cardiovascular Disease","authors":"Marina M. Bellet ,&nbsp;Francesco Curcio ,&nbsp;Luigi Frati ,&nbsp;Marilena Pariano ,&nbsp;Luigina Romani ,&nbsp;Massimiliano M. Corsi-Romanelli","doi":"10.1016/j.ajpath.2025.08.015","DOIUrl":"10.1016/j.ajpath.2025.08.015","url":null,"abstract":"<div><div>This review explores the emerging role of the gut microbiome in bridging autoimmunity and cardiovascular diseases. Dysbiosis, an imbalance in gut microbial composition, disrupts immune regulation, metabolic pathways, and vascular health, likely contributing to both autoimmune disorders and cardiovascular diseases. Microbial metabolites, such as short-chain fatty acids, trimethylamine N-oxide, tryptophan derivatives, and bile acids, play critical roles in modulating inflammation, lipid metabolism, and endothelial function. Specific bacterial species, including <em>Faecalibacterium prausnitzii</em>, <em>Akkermansia muciniphila</em>, and <em>Bifidobacterium</em> species., exhibit dual protective effects against autoimmune and cardiovascular pathologies. By elucidating these interconnected mechanisms, this work highlights the potential of microbiome-targeted therapies, such as probiotics, prebiotics, and dietary interventions, to concurrently address autoimmune diseases and reduce cardiovascular risk. Understanding the complex interactions between the gut microbiota, immune system, and cardiovascular health opens new avenues for developing innovative therapeutic strategies aimed at restoring microbial balance and improving patient outcomes.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 12","pages":"Pages 2288-2302"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay between Leptin and Stearoyl-CoA Desaturase 1 in Estrogen Receptor–Positive Breast Cancer Cells","authors":"Felice M. Accattatis ,&nbsp;Luca Gelsomino ,&nbsp;Linda Manna ,&nbsp;Piercarlo Del Console ,&nbsp;Laura Bianchi ,&nbsp;Alfonso Carleo ,&nbsp;Rossana De Salvo ,&nbsp;Lorenzo Arnaboldi ,&nbsp;Ludovica Baù ,&nbsp;Alberto Corsini ,&nbsp;Adele E. Leonetti ,&nbsp;Rocco Malivindi ,&nbsp;Marco Fiorillo ,&nbsp;Michael P. Lisanti ,&nbsp;Cinzia Giordano ,&nbsp;Daniela Bonofiglio ,&nbsp;Sebastiano Andò ,&nbsp;Stefania Catalano ,&nbsp;Ines Barone","doi":"10.1016/j.ajpath.2025.08.009","DOIUrl":"10.1016/j.ajpath.2025.08.009","url":null,"abstract":"<div><div>Obesity, a global health challenge, contributes to various cancers, including breast cancer. Complex metabolic dysregulation marks the development of both breast cancer and obesity. Here, the interplay between the obesity-derived adipokine leptin (LEP) and stearoyl-CoA desaturase 1 (SCD), a critical enzyme in fatty acid (FA) metabolism, was explored. While Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database analysis reported a significant protein-protein interaction between LEP and SCD, functional processing of the differentially expressed genes in LEP-treated breast cancer cells revealed a critical involvement of SCD in the interactome of deregulated proteins. Kaplan-Meier analyses linked LEP/SCD expression to poorer recurrence-free survival in patients with estrogen receptor α luminal A-like breast cancer. Functional studies demonstrated that LEP up-regulated SCD expression in luminal A-like breast cancer cells through LEP receptor-mediated signaling. Lipidomic profiling showed that SCD inhibition using MF-438 reduced LEP-induced FA desaturation, characterized by a shift from saturated to monounsaturated FAs. SCD inhibition also abolished the LEP-mediated mitochondrial respiration and ATP production. Additionally, LEP-induced oncogenic features, including enhanced growth and motility, were counteracted by pharmacologic/genetic SCD blockade, confirming SCD's role in leptin's protumorigenic effects. This study highlights the LEP-SCD axis as a driver of metabolic/functional alterations in estrogen receptor α–positive breast cancer, providing insights into the obesity–breast cancer link and identifying potential therapeutic targets (ie, SCD) to counter obesity-driven cancer progression.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 12","pages":"Pages 2492-2511"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"This Month in AJP","authors":"","doi":"10.1016/j.ajpath.2025.09.011","DOIUrl":"10.1016/j.ajpath.2025.09.011","url":null,"abstract":"","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 12","pages":"Page 2247"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145278845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KLF Transcription Factor 5/Lysophosphatidic Acid Receptor 5 Induced M2 Macrophage Activation and Inflammation by Modulating Phosphorylation of Mitogen-Activated Protein Kinase Kinase Kinase 7 in Pediatric Asthma","authors":"Jing Li ,&nbsp;Meixue Chen ,&nbsp;Lingling Lu ,&nbsp;Yinmiao Wang ,&nbsp;Wei Wu ,&nbsp;Yanhong Feng","doi":"10.1016/j.ajpath.2025.08.012","DOIUrl":"10.1016/j.ajpath.2025.08.012","url":null,"abstract":"<div><div>Pediatric asthma is a respiratory disease in which M2 macrophages play a critical role. Here, the role and molecular mechanism of lysophosphatidic acid receptor 5 (<em>LPAR5</em>) were investigated in pediatric asthma through <em>in vivo</em> and <em>in vitro</em> experiments. LPAR5 expression was increased in peripheral blood mononuclear cells from children with asthma. In an ovalbumin-induced neonatal asthmatic mouse model, LPAR5 antagonist alleviated airway inflammation by suppressing the release of inflammatory cytokines and inflammatory cell infiltration. Ovalbumin-induced M2 macrophage activation in neonatal mouse lung tissue was suppressed by LPAR5 antagonist, accompanied by decreased YM1 protein (encoded by chitinase 3 like 1) secretion. Differentiated THP-1 cells were stimulated with IL-4 to mimic M2 macrophages <em>in vitro</em>. M2 macrophage activation was reduced by both LPAR5 antagonist or LPAR5 knockdown. Furthermore, KLF transcription factor 5 (<em>KLF5</em>) was significantly up-regulated and positively correlated with LPAR5 expression in peripheral blood mononuclear cells from children with asthma. KLF5 bound to the promoter of LPAR5 and transcriptionally promoted LPAR5 expression. LPAR5 overexpression increased M2 macrophage activation in KLF5-depleted THP-1 cells. The underlying mechanism of LPAR5 was investigated by phosphorylomics analysis, which identified mitogen-activated protein kinase kinase kinase 7 as a possible downstream effector. The results showed that LPAR5 antagonist attenuated airway inflammation in neonatal mice by decreasing M2 macrophage activation. KLF5 positively regulates the expression of LPAR5, which further increased the phosphorylation of mitogen-activated protein kinase kinase kinase 7 protein in macrophages. This article highlights that LPAR5 might serve as a potential target in pediatric asthma.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"195 12","pages":"Pages 2320-2335"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145555249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}