Histology and histopathology最新文献

{"title":"The effect of intermittent fasting on liver morphology in non-alcoholic fatty liver disease: A narrative review of animal studies and clinical trials.","authors":"Katarzyna Piotrowska","doi":"10.14670/HH-25-081","DOIUrl":"10.14670/HH-25-081","url":null,"abstract":"<p><p>One of the more serious complications of obesity, apart from the development of type 2 diabetes, is the development of metabolic liver diseases, including non-alcoholic fatty liver disease (NAFLD). Intermittent fasting (IF) is one of the best-documented lifestyle changes in the literature, quickly improving metabolism and reducing inflammation. Meal consumption, its rhythm, and timing influence the functions of many organs, including the liver, whose main function is to respond to the nutrient load that occurs after a meal. The liver is an organ that responds rapidly to changes in nutritional intake. Even a single, episodic fast lasting longer than 10 hours triggers metabolic and epigenetic changes in the liver. Most studies observed a decrease in hepatic steatosis, most often described as a decrease in the number and size of fat droplets. Only in one study was an increase in the number of fat droplets observed. No improvement in liver morphology was observed in the case of low-choline diets. In models where hepatic steatosis levels were reduced, a reduction in inflammation was also observed, including fewer inflammatory cells in the liver and a reduction in fibrosis. Fasting is responsible for altering the components used for energy production. It also alters liver metabolism in pathways responsible for lipid and cholesterol metabolism, insulin signaling, circadian rhythm, and immune function. There are several types of IF, and each has its own benefits. Differences in their courses allow tailoring the intervention to individual lifestyles and socioeconomic circumstances, helping patients to persevere with the intervention and achieve the best results. There is also a need for further research, particularly clinical trials in larger, more diverse patient groups, to determine the full potential health benefits of IF.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1781-1790"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HNMT promotes the motility-associated structures of breast cancer cells through the PI3K/Akt signaling pathway to promote tumor progression.","authors":"Hong Liu, Jianhui Zhang, Yanjun Zhao, Ting Gao, Jianxin Li, Zhixiong Fan, Yongheng Yang, Jingyuan Yang, Ande Luo, Yi Zhao, Xin Chen, Cairui Li","doi":"10.14670/HH-25-074","DOIUrl":"10.14670/HH-25-074","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer (BC) is a tumor type that severely threatens the health and lives of women worldwide. Cancer cell motility often leads to the distant metastasis of BC. Histamine N-methyltransferase (HNMT) has been reported to be associated with poor prognosis in patients with BC; however, its role in BC cell motility remains unclear. Therefore, this study aimed to investigate the role of HNMT in BC cell motility.</p><p><strong>Methods: </strong>MDA-MB-231 cells were injected into the mammary fat pads of female BALB/c nude mice to establish a BC orthotopic tumor model, and BC lung metastasis was evaluated via HE staining. To investigate the effects of HNMT on the malignant behavior of BC cells, HNMT was knocked down or overexpressed in MDA-MB-231 cells. Cell proliferation, migration and invasion were analyzed by using CCK-8, scratch and Transwell assays, respectively. Moreover, the expression of key genes and proteins was detected via RT-qPCR, Western blotting, immunofluorescence and immunohistochemistry; additionally, the formation of invasive pseudopodia was detected via phalloidin staining.</p><p><strong>Results: </strong>HNMT expression was upregulated in BC. HNMT knockdown inhibited BC growth and lung metastasis <i>in vivo</i>. <i>In vitro</i>, HNMT knockdown inhibited MDA-MB-231 cell proliferation, migration, and invasion, as well as the formation of invasive pseudopodia and epithelial-mesenchymal transition (EMT), whereas the overexpression of HNMT exhibited the opposite effect, thus indicating that the upregulation of HNMT expression is associated with BC cell motility. In addition, HNMT was observed to activate the PI3K/AKT pathway. Treatment with the PI3K activator 740 Y-P alleviated the inhibitory effect of HNMT knockdown on the proliferation, migration, invasion, and EMT of MDA-MB-231 cells.</p><p><strong>Conclusion: </strong>HNMT promoted BC cell invasion and metastasis through the activation of the PI3K/AKT signaling pathway, thereby promoting the malignant progression and lung tumor metastasis of BC. This study provides novel insights and potential therapeutic strategies for BC treatment.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1839-1851"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular and clinicopathological characteristics of <i>NTRK</i> fusions in papillary thyroid carcinoma: Hospital experience with a literature review.","authors":"Hui Tang, Ting Sun, Jie Zhou, Huifang Zhang, Mingfeng Li, Zhiyin Xie, Yan Zhao","doi":"10.14670/HH-25-073","DOIUrl":"10.14670/HH-25-073","url":null,"abstract":"<p><p>Neurotrophic tyrosine receptor kinase (<i>NTRK</i>) fusions are rare but significant oncogenic drivers in papillary thyroid carcinoma (PTC). This study aims to delineate the clinicopathological and molecular characteristics of <i>NTRK</i> PTC and situate these findings within the current literature to advance diagnostic accuracy. Retrospective analysis of targeted next-generation sequencing (NGS) data from 66 primary thyroid cancer patients identified two female cases with <i>NTRK</i> fusions: a 22-year-old with <i>TPR::NTRK1</i> and a 53-year-old with <i>ETV6::NTRK3</i>, both validated by fluorescence in situ hybridization (FISH). The <i>TPR::NTRK1</i> patient presented with multifocal left-sided PTC, exhibiting lymph node metastasis (22/45), capsular invasion, multiple pulmonary nodules, and positive pan-TRK immunohistochemistry (IHC). Histologically, the tumor showed papillary architecture with invasive growth. The 12-month follow-up after total thyroidectomy, neck dissection, and radioactive iodine therapy (¹³¹I) showed no PTC recurrence and revealed calcified proliferative changes in the pulmonary nodules. The <i>ETV6::NTRK3</i> patient had a unifocal right-sided encapsulated PTC with no evidence of metastasis and negative pan-TRK IHC. Histology revealed a predominant follicular architecture with focal conventional papillary features. Following right hemithyroidectomy, no recurrence or metastasis was observed at the 24-month follow-up. This study highlights the importance of targeted NGS combined with FISH and clinicopathological analysis for accurate diagnosis in <i>NTRK</i> fusion PTC. While pan-TRK IHC is useful for initial screening, confirmatory NGS is essential to avoid false-negative results.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1829-1838"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Caloric restriction attenuates age-related liver and kidney alterations in mice: Histological evidence.","authors":"Carlos R Montes-de-Oca-Saucedo, Sheila A Villa-Cedillo, Cristina S Ríos-Vázquez, Eduardo A Álvarez-Tostado-Ojeda, Mario Murguía-Pérez, Eduardo Agustín-Godínez, Ricardo Ruiz-Salazar, Adolfo Soto-Domínguez, Odila Saucedo-Cárdenas","doi":"10.14670/HH-25-065","DOIUrl":"10.14670/HH-25-065","url":null,"abstract":"<p><strong>Objective: </strong>This study evaluated the histological impact of long-term caloric restriction (CR) on liver and kidney aging, assessing fibrosis, metabolic overload, and senescence-associated readouts.</p><p><strong>Methods: </strong>Eight-week-old male C57BL/6 mice were assigned to a standard diet (SD) or 50% CR and sacrificed at 12 or 16 months. A two-month-old group served as control (n=5/group). Liver and kidney tissues were processed for Hematoxylin and Eosin (H&E), Periodic Acid-Schiff (PAS), and Masson's Trichrome staining. Immunohistochemistry (IHC) assessed SIRT1, p16^INK4a, and acetylated p53 (Lys382) in both organs, and β-galactosidase immunoreactivity (IHC-DAB) in liver. Sections underwent morphometric quantification and statistical analysis.</p><p><strong>Results: </strong>Aged SD mice exhibited liver injury, increased PAS positivity, and collagen deposition, whereas CR attenuated these changes. The SD 16M group displayed the highest PAS positivity, while CR limited glycogen accumulation and preserved lobular architecture. In the kidney, SD animals developed tubular degeneration and architectural disruption; CR preserved renal structure and reduced tubular damage. CR was associated with higher SIRT1 immunoreactivity and lower acetylated p53, consistent with preserved SIRT1-linked deacetylation status. p16-positive cells increased with age under SD and were reduced by CR, though not fully normalized at 16 months. β-galactosidase immunoreactivity was evident in aged SD hepatocytes but minimal in CR groups.</p><p><strong>Conclusion: </strong>Long-term CR preserves hepatic and renal histoarchitecture during aging by limiting metabolic overload, fibrotic remodeling, and senescence, accompanied by a sustained SIRT1/acetyl-p53 profile consistent with reduced p53 activation.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1799-1814"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Kininogen 1/bradykinin receptor B2 system serves as a key molecular response of vancomycin-induced nephrotoxicity and may be a potential target of absinthin.","authors":"Shaoshan Zhou, Cuizhi Li, Zhihua Tang, Fengfeng Li, Jiangying Long","doi":"10.14670/HH-25-085","DOIUrl":"10.14670/HH-25-085","url":null,"abstract":"<p><strong>Objective: </strong>The occurrence of nephrotoxicity induced by Vancomycin (Van) has been documented in both experimental models and clinical patients. In this study, we aimed to identify potential gene targets by utilizing Gene Expression Omnibus (GEO) datasets and a Van-induced mouse model.</p><p><strong>Methods: </strong>Differentially expressed genes (DEGs) were filtered using GEO datasets (GSE7793), and a mouse model of nephrotoxicity was established by administering Van (400 mg/kg/day for 7 days) via intravenous injection.</p><p><strong>Results: </strong>A total of 485 DEGs were identified, consisting of 335 upregulated and 150 downregulated genes, based on the criteria of |Log2(fold change)| > 2 and <i>p</i>.adj < 0.05. Through the analysis of protein-protein interaction (PPI) networks, 15 hub genes were identified, suggesting that the kininogen 1 (<i>Kng1</i>)/bradykinin receptor B2 (<i>Bdkrb2</i>) system may play a central role in Van-induced nephrotoxicity. In our mouse model, Van treatment resulted in cell apoptosis and tubular injury in the kidney. The mRNA expression levels of <i>Kng1</i> and <i>Bdkrb2</i> were significantly increased in Van-treated mice compared with normal mice. Furthermore, we found that absinthin acts as a potential inhibitor of Bdkrb2 and effectively ameliorates Van-induced podocyte apoptosis and reduces the levels of renal injury biomarkers, including serum creatinine (Cre), blood urea nitrogen (BUN), and malondialdehyde (MDA).</p><p><strong>Conclusions: </strong>Our findings suggest that targeting Kng1/Bdkrb2 may offer a potential therapeutic strategy for mitigating Van-induced nephrotoxicity. These findings suggest that absinthin may serve as a renal protective agent against drug-induced nephrotoxicity.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1877-1889"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutamate signaling and transport around nodes of Ranvier and internodal myelin regions.","authors":"José Javier Miguel-Hidalgo","doi":"10.14670/HH-25-077","DOIUrl":"10.14670/HH-25-077","url":null,"abstract":"<p><p>The roles of glutamate as a major building block of proteins and as a key participant in numerous metabolic pathways are well established. Likewise, glutamate's function as a neurotransmitter-along with the distribution and actions of its receptors and reuptake mechanisms within the brain's gray matter-has been extensively characterized, leading to the development of existing and emerging treatments for neurological and psychiatric disorders. More recently, it has become clear that glutamate is also released in significant amounts within the white matter (WM), where it acts on specific receptors and is taken up by dedicated transporters. In the WM, glutamate is essential for activating receptors that support the development and maintenance of myelinated axons. Growing evidence further indicates that elevated extracellular glutamate or impaired glial reuptake in the WM can lead to pathological outcomes. Many of the receptors and transporters involved in glutamate signaling are located on astrocytic membranes and on the oligodendrocyte-derived myelin sheath, particularly concentrated at nodes of Ranvier and the adjacent paranodal and juxtaparanodal regions. This expanding understanding of glutamate-related mechanisms in the WM may ultimately pave the way for new therapeutic strategies targeting WM pathologies.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1773-1780"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histopathological and molecular mechanisms of multi-organ damage in heat stroke: Endothelial failure, immune crosstalk, and regulated cell death pathways.","authors":"Myoung Cheol Shin, Bo Hyun Jung, Joongbum Moon, Ji Hyeon Ahn, Jun Hwi Cho, Ki-Yeon Yoo, Moo-Ho Won","doi":"10.14670/HH-25-076","DOIUrl":"10.14670/HH-25-076","url":null,"abstract":"<p><p>Heat stroke is a life-threatening condition characterized by severe hyperthermia accompanied by central nervous system dysfunction and progressive multi-organ injury. Although rapid cooling remains the cornerstone of clinical management, accumulating evidence indicates that normalization of core body temperature alone does not fully prevent delayed organ damage. Experimental and clinical studies increasingly demonstrate that heat stroke-induced pathology extends beyond acute thermal injury and involves sustained endothelial dysfunction, coagulation imbalance, sterile inflammation, mitochondrial failure, and regulated cell death pathways. Histopathological analyses across multiple organs, including the brain, liver, kidneys, and intestine, reveal persistent microvascular injury, tissue edema, microthrombi formation, inflammatory infiltration, and cellular degeneration following the hyperthermic phase. These tissue-level alterations are closely linked to molecular mechanisms such as endothelial glycocalyx disruption, inflammasome activation, mitochondrial dysfunction, and dysregulated immune-coagulation crosstalk. Importantly, these interconnected processes form a self-amplifying injury network that contributes to delayed neurological deterioration and systemic organ failure despite effective cooling. This review integrates histopathological and molecular evidence from experimental models and human studies to provide a systems-level framework of post-hyperthermic injury in heat stroke. By linking tissue pathology with underlying mechanisms and translational therapeutic targets, this article highlights why cooling alone is insufficient and emphasizes the need for multimodal, mechanism-based interventions to mitigate delayed organ injury and improve clinical outcomes.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1755-1772"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xuebijing alleviates septic myocardial injury by inhibiting ferroptosis mediated by the ICAM1/TLR signaling pathway.","authors":"Xiaoyan Meng, Xinming Yan, Chen Kan, Haiquan Li, Dahe Han, Yi Guo, Peng Xue, Yuxin Jiang","doi":"10.14670/HH-25-079","DOIUrl":"10.14670/HH-25-079","url":null,"abstract":"<p><strong>Background: </strong>Xuebijing (XBJ) has demonstrated efficacy in alleviating clinical symptoms in sepsis patients; however, its underlying mechanism requires further investigation.</p><p><strong>Methods: </strong>In this study, we established mouse and cardiomyocyte sepsis models using LPS. Cardiac pathological changes and ICAM1 expression were assessed through HE staining and immunohistochemistry. The expression of ICAM1, TFR1, ASCL4, TLR1, TBK1, and IFR7 was analyzed via PCR and western blotting. Cardiomyocyte survival and apoptosis were evaluated using the MTT assay and flow cytometry, respectively. Additionally, cTnI, BNP, CK-MB, IL-1β, IL-6, and TNF-α levels, along with GSH and MDA levels, were measured.</p><p><strong>Results: </strong>HE staining confirmed the successful construction of the LPS-induced mouse model. XBJ inhibited ICAM1 expression in myocardial tissue as well as cells. Overexpression of ICAM1 suppressed survival and GSH levels while promoting apoptosis along with increased levels of cTnI, BNP, CK-MB, IL-1β, IL-6, TNF-α, and MDA of myocardial cells. Furthermore, ICAM1 activated Toll-like receptor (TLR) signaling pathways. Conversely, ICAM shRNA exhibited opposite effects. XBJ inhibited the overactivated TLR signaling pathway, inflammatory responses, and apoptosis induced by ICAM overexpression.</p><p><strong>Conclusion: </strong>XBJ ameliorates myocardial injury in sepsis by inhibiting the ICAM-regulated TLR signaling pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1865-1876"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SPI1-driven POSTN transcription promotes esophageal cancer progression and macrophage immunosuppressive polarization.","authors":"Hao Ding, Guanchu Liu, Xingqiang Ran, Bo Yang, Maoyong Fu","doi":"10.14670/HH-25-078","DOIUrl":"10.14670/HH-25-078","url":null,"abstract":"<p><strong>Background: </strong>Esophageal cancer (EC) is a common gastrointestinal cancer with the highest mortality. Studies have suggested that macrophages play a key role in cancer progression. Increasing evidence reveals that periostin (POSTN) is associated with the physiological and pathological processes in EC. However, the upstream mechanisms of POSTN on EC cell oncogenic properties and macrophages are still vague.</p><p><strong>Methods: </strong>qRT-PCR and western blotting were used to detect the mRNA and protein levels. Cell survival, migration, and invasion were determined using 5-ethynyl-2'-deoxyuridine, colony formation, flow cytometry, and Transwell assays. Macrophage infiltration and polarization were detected by Transwell assay and flow cytometry. The interaction between POSTN and Salmonella pathogenicity island 1 (SPI1) was verified using ChIP and dual-luciferase reporter assays. Xenograft models were established for <i>in vivo</i> assay.</p><p><strong>Results: </strong>POSTN was highly expressed in EC tissues and cells. The knockdown of POSTN suppressed EC cell growth, migration, and invasion, as well as eliminated macrophage infiltration and M2-like polarization, but induced M1-like activation. Mechanistically, SPI1 bound directly to the promoter region of POSTN and induced POSTN transcription. SPI1 expression was also increased in EC tissues. SPI1 silencing inhibited EC cell growth, migration, and invasion, and contained macrophage infiltration and M2-like polarization, while these effects were reversed by POSTN overexpression. <i>In vivo</i> assay showed that POSTN overexpression abolished SPI1-induced growth inhibition in EC xenografts.</p><p><strong>Conclusion: </strong>SPI1-driven POSTN transcription promotes EC cell growth and induces macrophage infiltration and immunosuppressive polarization, suggesting a new target for EC therapy.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1853-1863"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Digital quantitative analysis of <i>muscularis mucosae</i> thickness in early gastric cancer specimens reveals anatomical variation.","authors":"Tomoki Koike, Yukinobu Ito, Masafumi Horie, Takehito Kumata, Maki Sakaguchi, Hiroko Ikeda, Taro Yamashita, Daichi Maeda","doi":"10.14670/HH-25-084","DOIUrl":"10.14670/HH-25-084","url":null,"abstract":"<p><p>The <i>muscularis mucosae</i> (MM) is a thin layer of smooth muscle in the gastrointestinal tract that may act as a barrier against carcinoma invasion; however, its characteristics in gastric cancer remain unclear. This study aimed to precisely measure MM thickness in early gastric cancer and assess its association with anatomical location, mucosal atrophy, <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection status and cancer invasion. We analyzed 62 cases of early gastric cancer treated by endoscopic submucosal dissection (ESD), including 38 mucosa-confined (pT1a) and 24 submucosal-invasive (pT1b) cancers. The MM was visualized using desmin immunohistochemistry, and whole-slide imaging combined with digital image analysis enabled accurate quantification of MM thickness. The relationships between MM thickness and depth of invasion, tumor size, clinical parameters, anatomical location, mucosal atrophy and <i>H. pylori</i> infection were evaluated. No significant association was observed between MM thickness and cancer invasion, tumor size, or other clinical parameters. MM thickness was significantly greater in the pyloric antrum than in the gastric body and was thicker in the lesser curvature than in the greater curvature. In addition, MM thickness was significantly greater in cases with mucosal atrophy than in those without. Given the association between the presence of mucosal atrophy and increased MM thickness, together with the fact that the observed anatomical differences correspond to the distribution and progression of chronic gastritis, it is reasonable to speculate that chronic gastritis contributes to thickening of the MM.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1821-1828"},"PeriodicalIF":2.2,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}