Histology and histopathology最新文献

{"title":"Discordance of intrinsic subtype between primary tumor and lymph node metastasis in breast cancer patients.","authors":"Yoko Omi, Tomoko Yamamoto, Yoji Nagashima, Takako Kamio, Kiyomi Horiuchi, Takahiro Okamoto","doi":"10.14670/HH-18-989","DOIUrl":"10.14670/HH-18-989","url":null,"abstract":"<p><p>The heterogeneity of cancer cells between primary breast tumors and lymph node (LN) metastases at the initial therapy remains unclear. This study aimed to determine whether intrinsic subtypes of LN metastasis differ from those of primary breast tumors and how much additional information is obtained. Ninety-three breast cancer cases with LN metastasis were enrolled in the study. Immunohistochemistry for ER, PgR, HER2, and Ki-67 was performed for primary breast tumors and the largest LN metastases. The intrinsic subtype was determined as luminal A (ER⁺, PgR⁺, HER2^-, Ki-67 index &le;20%), luminal B (ER⁺, HER2^-, PgR^- or PgR⁺, and Ki-67 index >20%), luminal B HER2 rich (ER⁺, HER2⁺), HER2 (ER^-, HER2⁺), and triple-negative (ER^-, PgR^-, HER2^-). ). The discordance ratios for intrinsic subtypes between the primary tumor and LN metastasis were analyzed. The discordance ratios for ER, PgR, HER2, and Ki-67 were 0/93 (0%), 7/93 (7.5%), 2/93 (2.2%), and 10/93 (10.8%), respectively. The discordance ratio for the intrinsic subtype was 9/93 (9.7%). Considering the intrinsic subtype of LN metastasis, the effects of additional chemotherapy and anti-HER2 therapy could be expected in 4/93 (4.3%) and 1/93 (1.1%) patients, respectively. The discordance ratio for the intrinsic subtype between the primary breast tumor and LN metastasis was 9.7%. Considering the intrinsic subtype of LN metastasis, additional medical therapy could be expected to be effective in 5/93 (5.4%) breast cancer cases with LN metastasis. Immunohistochemistry of metastatic LNs may be useful for planning adjuvant therapy when the analysis of the primary site is inconclusive.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18989"},"PeriodicalIF":2.0,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085943","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":"Calycosin accelerates wound healing in diabetic rats by alleviating oxidative stress and promoting angiogenesis.","authors":"Wei Lu, Min Lu, Lifen Xue, Mi Zhou, Meifeng Zhang, Huifeng Zhu","doi":"10.14670/HH-18-987","DOIUrl":"https://doi.org/10.14670/HH-18-987","url":null,"abstract":"<p><strong>Background: </strong>Angiogenesis is a physiological process of diabetic wound healing. Although calycosin has been reported to exert protective effects on diabetic nephropathy, its role and mechanisms in diabetic wound healing remain unclear. This study investigates the effects of calycosin on wound healing and angiogenesis, and the role of the Nrf2/HO-1 pathway in mitigating oxidative stress in diabetic rats.</p><p><strong>Methods: </strong><i>In vivo</i>, type 2 diabetes (T2DM) in Sprague-Dawley (SD) rats was induced by a high-fat diet for six weeks combined with a single intraperitoneal injection of 45 mg/kg streptozotocin (STZ). The anesthetized diabetic rats underwent a full skin excision on the back and were then treated with calycosin for two weeks to evaluate the protective effect of calycosin on oxidative stress associated with the Nrf2/HO-1 pathway in diabetic wound rats. <i>In vitro</i>, damage to Human Umbilical Vein Vascular Endothelial Cells (HUVECs) was induced by high glucose, and then treated with calycosin or combined with Nrf2 agonist to evaluate whether calycosin affects cell activity and inhibits oxidative damage via the Nrf2/HO-1 pathway.</p><p><strong>Results: </strong>Our results indicate that calycosin promotes angiogenesis by activating the Nrf2/HO-1 signaling pathway and upregulating downstream antioxidant genes, thereby accelerating wound healing. <i>In vitro</i> studies have also shown that Nrf2/HO-1 signaling activation can enhance the promoting effect of calycosin on cell activity and the inhibitory effect on oxidative stress in HUVECs induced by high glucose.</p><p><strong>Conclusion: </strong>Our results show that calycosin can accelerate wound healing by promoting angiogenesis and inhibiting oxidative stress mediated by the Nrf2/HO-1 pathway, which provides a theoretical basis for the treatment of refractory diabetic wounds.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18987"},"PeriodicalIF":2.0,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080514","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":"Differential expression of ferroptosis markers, circadian regulators, KLOTHO, and classical tumor suppressors in colorectal cancer according to tumor stage: Influence of age, anatomical location, and correlation patterns.","authors":"Miguel A Saez, Cielo Garcia-Montero, Oscar Fraile-Martinez, Ana M Minaya-Bravo, Diego Liviu Boaru, Diego De Leon-Oliva, Patricia De Castro-Martinez, Majd N Michael Alhaddadin, Silvestra Barrena-Blázquez, Laura Lopez-Gonzalez, Luis G Guijarro, Natalio Garcia-Honduvilla, Víctor Roberto Baena Romero, Carlos Daniel Padilla Ansala, Mar Royuela, María Del Val Toledo Lobo, Leonel Pekarek, Roberto Fernández-Baillo Gallego de la Sacristana, Mauricio Hernández-Fernández, Montserrat Chao Crecente, Melchor Alvarez-Mon, Raul Diaz-Pedrero, Miguel A Ortega","doi":"10.14670/HH-18-988","DOIUrl":"https://doi.org/10.14670/HH-18-988","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a leading cause of cancer-related mortality, with an incidence projected to rise significantly worldwide. While TNM staging remains the cornerstone of prognosis and treatment decisions, additional biomarkers are needed to enhance predictive accuracy and therapeutic targeting. Ferroptosis, an iron-dependent cell death pathway, has emerged as a key regulator of CRC progression and therapy resistance. Circadian rhythms, KLOTHO, and tumor suppressors, such as p53, CDKN1A (p21), and Rb, also play crucial roles in CRC biology. Integrating TNM staging with molecular markers and patient-specific variables offers a more precise, personalized approach to CRC management. In the present work, we analyze the histopathological expression of KLOTHO, ferroptosis markers (TFRC, ALOX-5, ACSL-4, and GPX-4), circadian regulators (CLOCK, BMAL1, PER1, and PER2), and classical tumor suppressors (p53, p21, and Rb) in a cohort of 63 patients diagnosed with CRC. Besides, we have considered important clinical variables, like sex, age, and anatomical location, in our statistical analysis; correlation with the protein expression of these markers was also included for each stage (T1, T2, and T3). Our study reveals that advanced CRC stages (primarily T3) exhibit increased expression of ferroptosis markers (TFRC, ALOX5, ACSL4, and GPX4) and tumor suppressors (p53, p21, and Rb), alongside reduced histopathological detection of KLOTHO and circadian markers (BMAL1, CLOCK, PER1, and PER2) compared with earlier stages. Age, but not sex, influenced the expression of several markers. Tumor location also played a role, with right-sided CRCs showing significant stage-related differences in ferroptosis, tumor suppressor, and BMAL1, whereas left-sided tumors exhibited variations primarily in circadian markers (CLOCK, PER1, and PER2). Correlation analyses across tumor stages indicate dynamic shifts, with tumor suppressors maintaining positive associations with ferroptosis markers and anti-aging/circadian markers showing stage-dependent changes. Despite the inherent limitations of our study, these findings highlight the evolving biomarker landscape in CRC progression, although further research is needed to elucidate their clinical implications.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18988"},"PeriodicalIF":2.0,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075042","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":"Intermittent fasting-induced autophagy normalization confers hepatic protection in metabolic dysfunction-associated fatty liver disease: Mechanistic insights and implications.","authors":"Payal Bhatnagar, Gehan El-Akabawy, MoezAlIslam E Faris, Manoj B Menon, Mohamed Abdel Wahab, Farida Hussan, Mohd Hazim Bin Zulkaflee, Nabil Eid","doi":"10.14670/HH-18-986","DOIUrl":"https://doi.org/10.14670/HH-18-986","url":null,"abstract":"<p><p>Metabolic dysfunction-associated fatty liver disease (MAFLD) is a chronic liver condition that can progress to steatohepatitis, cirrhosis, and even liver cancer. Macroautophagy (hereinafter referred to as autophagy) is a pro-survival mechanism that facilitates the lysosomal clearance of damaged organelles, abnormal proteins, and excess lipids. A growing body of evidence indicates that autophagy dysfunction and reduced autophagic flux play critical roles in the pathogenesis of MAFLD. Therefore, restoring autophagy in MAFLD may help reduce steatosis and prevent disease progression. Intermittent fasting (IF), involving periods of restricted to no food intake alternating with periods of regulated/free eating, has been demonstrated to have beneficial effects on body composition, glucose regulation, lipid profiles, and liver function in studies involving both animal models of MAFLD and human subjects. Studies involving individuals with obesity and MAFLD have shown that Ramadan intermittent fasting (RIF), an Islamic religious practice that involves abstaining from food and water intake from sunrise to sunset over approximately 30 consecutive days, significantly reduces body weight, BMI, fat mass, and inflammatory markers while improving liver function and steatosis. The hepatoprotective effects of RIF are associated with the enhanced expression of autophagy-related genes and the restoration of autophagic flux. This upregulation of autophagy as a result of RIF makes it a potentially promising therapeutic strategy for MAFLD. This review summarizes various forms of IF, the mechanisms of autophagy, and evidence of autophagy dysfunction in MAFLD. It also explores how IF, specifically RIF, may normalize autophagy, reduce hepatic steatosis, and improve liver function in human subjects.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18986"},"PeriodicalIF":2.0,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145064704","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":"Tumor promotion or suppression: Revisiting the role of EXT1 and Heparan sulfate.","authors":"Ayumi Niwa, Hiroyuki Tomita, Akira Hara","doi":"10.14670/HH-18-985","DOIUrl":"https://doi.org/10.14670/HH-18-985","url":null,"abstract":"<p><p>Heparan sulfate (HS), a linear sulfated polysaccharide attached to proteoglycans, modulates the availability and activity of growth factors and cytokines to regulate cell signaling, adhesion, and migration. Exostosin-1 (EXT1), a key glycosyltransferase for HS chain elongation, is increasingly implicated in cancer development and progression. Although originally identified as a tumor suppressor in hereditary multiple exostoses, EXT1 exhibits a complex, context-dependent role in cancer. The effects of EXT1 in cancer differ by cell and tumor type, exerting both tumor-suppressing and tumor-promoting effects. Notably, EXT1 also alters the tumor microenvironment via its expression in stromal fibroblasts and endothelial cells, further influencing tumor behavior. This review discusses the functions of HS and EXT1, emphasizing the roles of EXT1 in cancer and its microenvironment. A deeper understanding of these mechanisms may offer novel therapies targeting the HS biosynthetic pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18985"},"PeriodicalIF":2.0,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039996","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":"Guishen-erxian Decoction can improve ovarian function in rats with premature ovarian failure by inhibiting oxidative stress and granulosa cell DNA fragmentation mediated by the PI3K/Akt/FOXO3a pathway.","authors":"Huanmei Zhong, Yuhua He, Wenhui Wang, Yingyun Liu, Danna Chen, Yongqi Shen, Chengjie Liang","doi":"10.14670/HH-18-984","DOIUrl":"https://doi.org/10.14670/HH-18-984","url":null,"abstract":"<p><strong>Background: </strong>The aim of this study was to establish a rat model of premature ovarian failure (POF) with cyclophosphamide (CTX), and explore the molecular basis of POF and the mechanism of Guishen-Erxian Decoction (GSEXD) to improve POF from the perspective of oxidative stress regulation of ovarian granulosa cell (OGC) DNA fragmentation.</p><p><strong>Method: </strong>The study utilized SD rats to establish a POF model via CTX. Rats were divided into Control, POF group, three GSEXD dosage groups (low, medium, high), and a GSEXD+PI3K agonist group to assess GSEXD's therapeutic effects on oxidative stress, DNA fragmentation and ovarian damage.</p><p><strong>Result: </strong>GSEXD can improve the body weight, ovarian index, pathological status, and hormone secretion of POF rats, and inhibit ovarian oxidative stress and DNA fragmentation. In addition, GSEXD inhibits the activation of the PI3K/Akt/FoxO3a pathway. PI3K agonist 740 Y-P can reverse the effects of GSEXD on ovarian function, ovarian antioxidant capacity, and granulosa cell DNA fragmentation in POF rats.</p><p><strong>Conclusion: </strong>Inhibition of oxidative stress damage and excessive DNA fragmentation of granulosa cells is a key pathway for GSEXD to promote follicle growth and development and alleviate ovarian function decline, which may be related to the inhibition of the PI3K/AKT/FOXO3a pathway by GSEXD.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18984"},"PeriodicalIF":2.0,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033300","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":"Microscopic studies on the structure of microornamentation and adhesive setae in normal and regenerating tail scales of some geckos.","authors":"Antonio Bonfitto, Lorenzo Alibardi","doi":"10.14670/HH-18-983","DOIUrl":"10.14670/HH-18-983","url":null,"abstract":"<p><p>The present review summarizes recent information on the formation and fine structure of epidermal microornamentation and adhesive setae in scale pads of the tail in some arboreal geckos. The study utilizes transmission and scanning electron microscopy, in conjunction with immunolabeling, to detect the main proteins of the microornamentation, known as Corneous Beta Proteins. These are special small proteins with a central region containing beta-sheets that form most of the corneous material of scales and pads. These proteins are packed into long cords that form short spinulae or longer setae. In tail scales, the spinulae feature different shapes but possess a limited size, 0.5-2.0 µm. In sparse areas located toward the distal part of the tail, some scales form adhesive pads, and their microornamentation grows longer, forming setae of 10-30 µm in length in the species studied herein. This process gives rise to stiff but flexible bristles that arboreal geckos use for adhesion on vertical or inverted substrates or tree branches. During tail regeneration, some scales also regenerate the adhesive setae and give rise to new adhesive pads. Caudal setae are formed by a process similar to that observed during the formation of digital setae. This derives from the interaction of a specific epidermal layer (clear) with another layer (Oberhäutchen), which are formed in the scale pads. Setae vary in length, diameter, or terminal arborization, and they resemble those of the digits, albeit shorter. The presence of caudal adhesive pads reinforces the prehensibility and maneuverability of these arboreal lizards in their environment.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18983"},"PeriodicalIF":2.0,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029573","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":"Brazilin attenuates kidney ischemia-reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction.","authors":"Jinyi Zhao, Lulu Zhang, Fei Mu, Ying Yu, Chen Cui, Meng Tang, Kexin Sun, Yanping Yin, Jingwen Wang, Rui Gong","doi":"10.14670/HH-18-982","DOIUrl":"https://doi.org/10.14670/HH-18-982","url":null,"abstract":"<p><p>Brazilin, a natural homoisoflavonoid, is the primary bioactive ingredient derived from the bark and heartwood of <i>Caesalpinia sappan</i> L. It has been proven to exhibit multiple biological activities and therapeutic potential in chronic degenerative diseases, fibrotic disorders, inflammatory diseases, and cancers. However, whether it is involved in regulating the pathological process of acute kidney injury (AKI) is not fully understood. This study aimed to elucidate the role and key pharmacological molecular mechanisms of brazilin in AKI. Our data demonstrated that pretreatment with brazilin can significantly reduce the high expression of serum creatinine (Scr), blood urea nitrogen (BUN), and lipocalin-2 (LCN2) in mice exposed to ischemia/reperfusion (I/R) and alleviate kidney histopathological damage. Meanwhile, pretreatment with brazilin can alleviate apoptosis, inflammation, and oxidative stress injury in the kidney tissue cells by partially inhibiting the Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB)/NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammatory pathway or activating the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) antioxidant pathway. <i>In vitro</i>, pretreatment with brazilin significantly downregulated pro-apoptotic Bax and upregulated anti-apoptotic Bcl-2 expression in human renal proximal tubular cells (HK-2) subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). Besides, it ameliorated mitochondrial dysfunction by enhancing mitochondrial biogenesis and restoring mitochondrial membrane potential. These effects collectively suppressed oxidative stress injury and NLRP3 inflammasome signaling pathway activation. In summary, brazilin exhibits significant protective effects against I/R-induced AKI by attenuating inflammation, oxidative stress and cell apoptosis, and mitochondrial damage. These findings suggest that brazilin holds promise as a potential therapeutic agent for AKI.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18982"},"PeriodicalIF":2.0,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023165","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":"CD63 is a diagnostic marker of prostate cancer and a prognostic marker of biochemical progression following radical prostatectomy.","authors":"Elisabeth Dingendorf, Marit Bernhardt, Isabella Federica Bollen, Tobias Kreft, Anna Katrin Scherping, Xiaolin Zhou, Manuel Ritter, Jörg Ellinger, Carsten Stephan, Glen Kristiansen","doi":"10.14670/HH-18-981","DOIUrl":"https://doi.org/10.14670/HH-18-981","url":null,"abstract":"<p><strong>Aims: </strong>We aimed to analyze CD63, a cell surface protein that has been associated with tumor aggressiveness in several cancers, including breast, colorectal, and lung cancer, as well as melanoma, in prostate cancer.</p><p><strong>Methods: </strong>CD63 expression was analyzed immunohistochemically in a cohort of primary prostate cancers from 281 patients. The results were correlated with clinico-pathologic parameters, including biochemical recurrence. In addition, CD63 expression in 251 of the 281 patients with prostate cancer was compared with CD63 expression in matched benign tissue samples (490 tissue samples). The analysis was performed automatically using the open-source software QuPath^© and tested for statistical significance. For comparison with the diagnostic markers AMACR and GOLPH2, CD63 was analyzed in an additional cohort of 198 Prostate cancers.</p><p><strong>Results: </strong>CD63 expression was found in 100% of prostate cancer cases and benign tissue spots. Increased CD63 expression was significantly associated with higher tumor stage (pT), tumor grade (ISUP), as well as shorter progression-free survival (PFS). Compared with the CD63 intensity of benign tissue, expression in tumor tissue was higher in >80% of cases. In addition, combining the expression of CD63 and AMACR, positivity reached 97.2%, making CD63 a promising diagnostic biomarker in challenging cases.</p><p><strong>Conclusions: </strong>CD63 is commonly overexpressed in prostate cancer, and higher levels are associated with earlier biochemical tumor progression; hence, CD63 is a promising diagnostic and prognostic biomarker in primary prostate cancer.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18981"},"PeriodicalIF":2.0,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015044","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":"Lactylation formation, gene regulation, biological functions, and clinical relevance.","authors":"Xiaoyu Wei, Zhimei Qiu, Youyang Huang, Qing Guo, Ying Li, Yongchao Zhao, Bei Shi","doi":"10.14670/HH-18-980","DOIUrl":"https://doi.org/10.14670/HH-18-980","url":null,"abstract":"<p><p>Lactate, as an end-product of glycolysis, has been considered as a metabolic waste that participates in a few physiological functions. Recently, a novel study by Zhao's laboratory reported that lactate can serve as an epigenetic modification substrate, causing histone or nonhistone lysine residues to undergo lactylation, which then regulates gene transcription, translation, and protein function. Subsequent studies confirmed that lactylation plays an important role in a series of physiological and pathological processes, such as inflammation, cancer, and other biological processes. In this review, we summarize advanced achievements on the effects of lactylation in various diseases and potential treatment targets, providing a reference and direction for future research.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18980"},"PeriodicalIF":2.0,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000418","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}