Journal of Molecular Histology最新文献

{"title":"Localization and function of APC15 during mouse oocyte meiotic progression","authors":"Shi-Bin Chao,&nbsp;Ren-Ren Zhang,&nbsp;Qing-Yuan Sun","doi":"10.1007/s10735-025-10404-8","DOIUrl":"10.1007/s10735-025-10404-8","url":null,"abstract":"<div><p>The Anaphase-Promoting Complex/Cyclosome (APC/C) is a critical regulator of cell cycle progression, with APC15 serving as an essential subunit. While the role of APC15 in mitosis is well characterized, its function during meiosis remains poorly understood. In this study, we investigated the expression, subcellular localization, and potential role of APC15 during mouse oocyte meiotic progression. Using immunofluorescence and confocal microscopy, we observed dynamic changes in APC15 localization throughout meiotic progression. Knockdown of APC15 via siRNA did not affect spindle organization, but led to meiotic arrest at metaphase I (MI) and impaired the removal of BUB3 from kinetochores, suggesting a disruption in Spindle Assembly Checkpoint (SAC) inactivation. Our results highlight the involvement of APC15 in the regulation of SAC and the transition from metaphase to anaphase in oocytes. These findings contribute to our understanding of APC15’s role in meiotic regulation and provide insights into its potential impact on maintaining chromosomal stability during oocyte maturation.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143716934","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":"Efficacy of curcumin-selenium nanoemulsion in alleviating oxidative damage induced by aluminum chloride in a rat model of Alzheimer’s disease","authors":"Safaa M. Awad,&nbsp;Yasser A. Attia,&nbsp;Hassan ElSayed,&nbsp;Shams H. Abdelhafez,&nbsp;Akaber T. Keshta,&nbsp;Eman Rashad,&nbsp;Heba M. A. Khalil,&nbsp;Aziza T. Fathy","doi":"10.1007/s10735-025-10406-6","DOIUrl":"10.1007/s10735-025-10406-6","url":null,"abstract":"<div><p>Alzheimer’s disease (AD) is a common neurological disorder primarily affecting older adults. A hallmark of this condition is the generation of reactive oxygen species (ROS), leading to increased oxidative stress and cellular damage. Treatment with a curcumin-selenium nanoemulsion has been shown to enhance behavioural performance and mitigate degenerative changes induced by aluminium chloride (AlCl₃). This nanoemulsion also reduced the activity of acetylcholinesterase (AChE) and lowered levels of key proteins, including Aβ, p53, tau, nuclear factor erythroid 2-related factor 2 (Nrf2), and tumour necrosis factor-alpha (TNF-α). Additionally, it significantly decreased nitric oxide (NO) levels in the brain while enhancing the activity of catalase (CAT) and superoxide dismutase (SOD). The study highlights the antioxidant and anti-inflammatory properties of the curcumin-selenium nanoemulsion, suggesting its potential as a therapeutic option for alleviating AD induced by AlCl₃. These results are further supported by improvements in the histological structure of the cortex and hippocampus, as well as enhanced immunohistochmical assessment of glial fibrillary acidic protein (GFAP). Cur- Se-nanoemulsion, the current drug delivery technology, may lower the amount of amyloid-β in AD rat brain and considerably ameliorate the memory deficit that improve therapy efficacy in AD lesions.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143716989","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":"Electron microscopic analysis of pomegranate and black chokeberry effects on acute pancreatitis in rats","authors":"E. Rumeysa Hekimoglu,&nbsp;Mukaddes Esrefoglu,&nbsp;Seda Kirmizikan,&nbsp;Huri Dedeakayogullari,&nbsp;Ozge Pasin,&nbsp;Birsen Elibol","doi":"10.1007/s10735-025-10380-z","DOIUrl":"10.1007/s10735-025-10380-z","url":null,"abstract":"<div><p>Despite numerous experimental and clinical studies in terms of novel therapeutic strategies, the treatment of acute pancreatitis (AP) is still symptomatic. In the present study, we aimed to evaluate the effects of <i>Punica-granatum L</i>. (pomegranate) and <i>Aronia-melanocarpa</i> (black chokeberry) which both have antioxidant and anti-inflammatory actions on the treatment of AP. Thirty-two rats were divided into 4 groups: Control, AP, pomegranate, and black chokeberry groups. To create AP, L-arginine was administered intraperitoneally. The rats from the pomegranate and black chokeberry groups were administered two doses of pomegranate and black chokeberry extract orally after each L-arginine injection for 7 days. Pancreatic tissues were processed for light and electron microscopic and biochemical evaluations. L-arginine administration resulted in severe necrotic AP characterized by necrosis, apoptosis, and significant increases in serum amylase, and lipase levels as well as tissue total oxidant status (TOS) levels. Degenerated organelles, apoptotic bodies, and myelinic figures were observed by electron microscopic examination. Both pomegranate and black chokeberry had beneficial effects on the treatment of AP via decreasing total histopathological damage score, apoptosis rate, and serum and tissue TOS levels. These beneficial effects of pomegranate and black chokeberry extracts may offer compelling information that may inspire and guide the development of novel therapeutic approaches for the treatment of AP.</p><h3>Graphical abstract</h3>\u0000<div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143698684","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":"In vivo and in silico analysis of anti inflammatory, antipyretic and analgesic activity of methanolic extract of Nigella sativa","authors":"Nureen Zahra,&nbsp;Saher Fatima,&nbsp;Anum Nazir,&nbsp;Syeda Yumna Farrukh,&nbsp;Ayesha Anwer,&nbsp;Abid Sarwar,&nbsp;Tariq Aziz,&nbsp;Fahad Al Asmari,&nbsp;Aziza Mahdy Nahari,&nbsp;Rewa S. Jalal,&nbsp;Fakhria A. Al-Joufi,&nbsp;Maher S. Alwethaynani","doi":"10.1007/s10735-025-10399-2","DOIUrl":"10.1007/s10735-025-10399-2","url":null,"abstract":"<div><p><i>Nigella Sativa</i> (<i>N. sativa</i>) belongs to the family of Ranunculaceae and is an annual herb which is also known as black cumin or black seed. Since ancient times <i>N. sativa</i> has been used because of its widespread therapeutic properties which has been proven effective in respiratory, cardiovascular, gastrointestinal, inflammatory conditions and in inflammation. This study investigates the antiinflammatory, antipyretic, and analgesic properties of <i>Nigella sativa</i> (<i>N. sativa</i>) methanol extract using albino rats (n = 36). Diclofenac and paracetamol were used as standard medications in the trial, and the four concentrations of the methanolic extract (250, 500, 1000, and 2000 mg/kg) were tested for their effects on inflammation, pain, and fever. The methanolic extract of <i>N. sativa</i> seeds showed significant inhibition of fever (96%), inflammation (89%), and pain (85%). In addition, bioactive compounds in the seeds, including thymol, p-cymene, and limonene, were examined through <i>in-silico</i> studies. Ligand molecules and proteins associated with anti-inflammatory, analgesic, and antipyretic effects were 1DFN, 1A06, and 3LN0, respectively. The molecular docking results indicated significant binding interactions, with effective binding energy values corresponding to analgesic, antipyretic, and anti-inflammatory properties. Both in-silico and in-vivo results demonstrate the efficacy of <i>N. sativa</i> methanol extract in alleviating pain, inflammation, and fever.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676413","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":"Ramipril ameliorates endometriosis by inducing oxidative stress-mediated apoptosis in the wistar rat","authors":"Piyali Mazumdar,&nbsp;Shampa Sarkar Biswas","doi":"10.1007/s10735-025-10397-4","DOIUrl":"10.1007/s10735-025-10397-4","url":null,"abstract":"<div><p>Endometriosis is illustrated by the presence of ectopic endometrial cells capable of evading apoptosis outside the uterus. Apoptotic and anti-apoptotic factors in the extra uterine microenvironment can be compromised by the impairment in oxidative status. Angiotensin Converting Enzyme (ACE) Inhibitors and Nitric Oxide (NO) modulators play pivotal role in inflammation, angiogenesis, apoptosis and in abrogating oxidative imbalance. Therefore, in the current study we investigate the role of ACE inhibitor and or NO modulators in mitigating the proliferation of ectopic endometrial lesions in rat model. Sixty adult female virgin wistar rats were utilized; out of which fifteen were used as donor rats and rest forty-two were randomly divided into seven groups after surgical implantation of endometrial explants into rats (group II–VII). Histomorphometric assessment of uteri and ectopic lesions was performed by Hematoxylin and eosin (H-E) staining, followed by immunohistochemical study for Proliferating cell nuclear antigen (PCNA), Bax and Bcl-2. Oxidative stress parameters were evaluated by biochemical estimations, succeeded by immunoblotting of Poly [ADP-ribose] polymerase 1 (PARP1). Additionally, immunoblotting of Vascular endothelial growth factor (VEGF), Bax, Bcl-2 and caspase-3 was also performed. Significant decrease in the diameter of lesions with diffused staining at the extracellular spaces of stromal cells for PCNA accompanied by significant decrease in the expression of VEGF (<i>p</i> &lt; 0.00001) was observed in group III. Furthermore, increased expression of Bax:Bcl-2 ratio (<i>p</i> &lt; 0.001) and cleaved caspase-3 (<i>p</i> ≤ 0.0001) in ectopic lesions of group III was also observed. Administration of ramipril alone results in triggering oxidative stress mediated cleavage of PARP1, augmenting apoptosis in the ectopic lesions.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676403","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":"miR-378d suppresses gastric cancer metastasis by targeting METTL4 to inhibit epithelial-mesenchymal transition","authors":"Danjie Xing,&nbsp;Jiapeng Bao,&nbsp;Jiancheng He,&nbsp;Hanxu Gao,&nbsp;Wanjiang Xue,&nbsp;Junjie Chen,&nbsp;Jia Li","doi":"10.1007/s10735-025-10392-9","DOIUrl":"10.1007/s10735-025-10392-9","url":null,"abstract":"<div><p>Metastasis is a major determinant of prognosis in gastric cancer (GC), and microRNAs (miRNAs) play crucial roles in driving the metastatic process. This study aimed to identify key miRNAs involved in GC metastasis and elucidate their underlying mechanisms. GC tissues from patients with and without metastasis were subjected to miRNA sequencing to identify differentially expressed miRNAs. Expression differences between GC and normal tissues, as well as their correlation with patient survival, were analyzed using data from The Cancer Genome Atlas and an internal cohort. miR-378d expression was measured by RT-qPCR in the internal cohort, and its association with clinicopathological features and prognosis was analyzed. Gene Set Enrichment Analysis (GSEA) was performed to investigate the potential mechanisms by which miR-378d influences GC metastasis. The findings were validated through in vitro wound healing, transwell assays, western blotting, and immunofluorescence, as well as in vivo models. MiRNA sequencing identified miR-378d as significantly downregulated in GC tissues and associated with poor prognosis. GSEA showed that miR-378d was negatively correlated with epithelial-mesenchymal transition (EMT). In vitro and in vivo experiments demonstrated that upregulation of miR-378d inhibited GC cell migration and invasion. Mechanistically, miR-378d suppressed EMT by downregulating METTL4 expression. miR-378d inhibits GC metastasis by suppressing EMT through the downregulation of METTL4, offering novel insights into the role of miRNAs in GC progression and highlighting potential therapeutic targets for intervention.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143667980","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":"Taraxasterol attenuates inflammatory responses in a 2,4-dinitrochlorobenzene-induced atopic dermatitis mouse model via inactivation of the MAPK and NF-κB pathways","authors":"Yu Zhang,&nbsp;Guoping Peng,&nbsp;Rusheng Zhang","doi":"10.1007/s10735-025-10391-w","DOIUrl":"10.1007/s10735-025-10391-w","url":null,"abstract":"<div><p>Atopic dermatitis (AD) is an inflammatory skin disease. Taraxasterol has anti-inflammatory effects in various pathological processes. In this study, our goal is to detect the biological functions of taraxasterol and its related mechanisms in AD development. The mouse model of experimental AD was established through application of 2’,4-dintrochlorobenzene (DNCB) onto the mouse dorsal skin. Taraxasterol (2.5, 5, and 10 mg/kg) was orally administrated to AD mice. Effects of taraxasterol on AD-like skin symptoms were examined through assessment of ratios of skin lesion area/dorsal skin region, skin thickness, skin hydration, and starching number. Histopathological changes were detected by performing H&amp;E staining. ELISA kits were obtained to measure serum TNF-α and IgE levels. RT-qPCR was conducted to measure mRNA levels of proinflammatory factors. Expression of MAPKs and NF-κB signaling was evaluated by western blotting. Taraxasterol alleviated AD-like skin symptoms (erosions, erythema, scaling, dryness, pruritus) and reduced lesion area and skin thickness in mice with DNCB-induced AD. Taraxasterol decreased epidermal thickness and serum levels of IgE and TNF-α and prevented the release of proinflammatory factors in lesion sites in of DNCB-induced AD mice. Mechanistically, taraxasterol inactivated the MAPK and NF-κB pathways. Taraxasterol alleviates AD-like skin symptoms and inflammation in a DNCB-induced AD mouse model via inactivation of the MAPK and NF-κB pathways.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143667981","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":"Notch 2 from bone marrow mesenchymal stem cells alleviates smoke inhalation-induced lung injury by mediating alveolar cell differentiation","authors":"Cunping Yin,&nbsp;Xiaoyan Wang,&nbsp;Yanmei Tao,&nbsp;Xiaoqing Wu,&nbsp;Yuan Li,&nbsp;Haiping Li,&nbsp;Yuan Liang","doi":"10.1007/s10735-025-10393-8","DOIUrl":"10.1007/s10735-025-10393-8","url":null,"abstract":"<div><h3>Background</h3><p>Smoke inhalation-induced lung injury (SILI) is the major fatality in fire- and blast-related accidents. Bone marrow mesenchymal stem cells (BMSCs) have a potential therapeutic role in SILI through directional differentiation into AT1, AT2, and pulmonary vascular endothelial cells. The present study proposes to evaluate the effect of Notch 2 on the directional differentiation of BMSCs and to characterize its reparative role in a SILI model.</p><h3>Methods</h3><p>pGMLV-SC5 RNAi and pcDNA 3.1 lentivirus exogenously regulate Notch 2 expression in rat-derived BMSCs and BMSCs were injected into the tail vein of the SILI rat model. H&amp;E, Masson and TUNEL stains characterized pathological changes in rat lung tissue. ELISA, western blot, and RT-qPCR identified inflammatory factors (IL-1β, IL-6 and TNF-α), Notch 2 pathway- (Notch 2 and Hes1), lung fibrosis- (α-SMA and E-cadherin), AT1- (AQP5), and AT2- (SPC and SPD) associated markers.</p><h3>Results</h3><p>pGMLV-SC5 RNAi or pcDNA 3.1 lentivirus could decrease or increase Notch 2 expression in BMSCs. In vivo imaging showed that BMSCs could be localized in the lungs of the SILI model at 24 h after model development. Treatment with BMSCs alleviated diffuse congestion, lung fibrosis, and alveolar cell apoptosis in lung tissues of the SILI model. Treatment of BMSCs decreased the levels of IL-1β, IL-6, TNF-α, and α-SMA and increased the expression of Notch 2, Hes1, E-cadherin, AQP5, SPC, and SPD in the SILI model. Overexpression of Notch 2 enhances the therapeutic effect of BMSCs on lung injury in the SILI model. Notably, overexpression of Notch 2 attenuated the BMSCs-induced upregulation of AQP5 expression and enhanced the BMSCs-induced upregulation of SPC and SPD expression.</p><h3>Conclusion</h3><p>Notch 2 contributes to lung injury repair in the SILI rat model by facilitating the differentiation of BMSCs to AT2. This study provides a new idea and target for the treatment of BMSCs for SILI.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143667990","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":"Direct exposure with exogenous mitochondria reduce colistin-induced mitochondrial dysfunction and cellular damages in isolated rat renal proximal tubular cells","authors":"Abdollah Arjmand,&nbsp;Ahmad Salimi,&nbsp;Maryam Mohammadabadi,&nbsp;Mehrdad Faizi,&nbsp;Amir Fakhri,&nbsp;Zhaleh Jamali,&nbsp;Jalal Pourahmad","doi":"10.1007/s10735-025-10389-4","DOIUrl":"10.1007/s10735-025-10389-4","url":null,"abstract":"<div><p>Kidney damage caused by colistin (polymyxin E) can bring about a decrease in creatinine clearance, potential proteinuria, cylindruria and oliguria in treated patients. It is therefore imperative to develop a new therapeutic strategy for reducing kidney damage after treatment with colistin. Mitochondrial damage is one of contributing factors in colistin-induced nephrotoxicity. Given the therapeutic benefits of mitochondrial transplantation by exogenous healthy mitochondria, we hypothesized that this strategy would be capable of ameliorating renal proximal tubular cells damage following exposure with colistin. For this purpose, we isolated rat renal proximal tubular cells (RPTCs) form kidney and exposed them with toxic concertation of colistin with/without rat healthy isolated mitochondria for 4 h. Cellular parameters such as lactate dehydrogenase (LDH), reactive oxygen species (ROS) formation, mitochondrial membrane potential (MMP), caspase 3 activation, lysosomal damage, glutathione and ATP content were measured. The results showed that administration of isolated mitochondria could improve colistin-induced nephrotoxicity and reduce mitochondrial dysfunction. Exogenous mitochondria reduced the activity of LDH, production of ROS, ATP and GSH depletion, loss of MMP, lysosomal damages and cell death. To the best of our knowledge, these results provide the first direct experimental evidence that direct exposure with exogenous mitochondria is capable of ameliorating cellular damage following treatment with colistin. These findings support that mitochondrial transplantation may be a promising therapeutic strategy for colistin-associated mitochondrial dysfunction in kidney cells.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143667989","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":"Serum proteomic profiling reveals potential predictive indicators for coronary artery calcification in stable ischemic heart disease","authors":"Haiyan Wu,&nbsp;Mingjie Pang,&nbsp;Haoqiang Chen,&nbsp;Ke Zhuang,&nbsp;Hong Zhang,&nbsp;Yan Zhao,&nbsp;Xiaoxue Ding","doi":"10.1007/s10735-025-10388-5","DOIUrl":"10.1007/s10735-025-10388-5","url":null,"abstract":"<div><p>Coronary artery calcification (CAC) is a common complication in patients with stable ischemic heart disease (SIHD). However, the early diagnosis and understanding of the pathogenesis of CAC in SIHD patients remain underdeveloped. This study aimed to analyze aberrant alterations in the serum proteome of SIHD patients, as well as SIHD patients with severe CAC (CAC_SIHD), and to explore the potential risk factors of CAC in SIHD patients. Serum proteomic profiles were obtained from individuals with SIHD (n = 6), CAC_SIHD (n = 6), and healthy controls (n = 9), and were analyzed using nano liquid chromatography tandem mass spectrometry (LC–MS/MS). The aberrant alterations in proteins and immune cells in the serum of SIHD and CAC_SIHD patients were characterized through differential protein expression analysis and single-sample gene set enrichment analysis analysis, respectively. Differentially expressed proteins (DEPs) were further subjected to gene ontology functional enrichment and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. Finally, Receiver Operating Characteristic analysis was performed on the DEPs between SIHD and CAC_SIHD to identify potential predictive factors of CAC. Abnormalities in multiple complement pathways and lipid metabolism were observed in SIHD and CAC_SIHD patients. Moreover, SIHD and CAC_SIHD were characterized by an increased presence of T cells and natural killer cells, along with a reduced presence of B cells. Subsequent analysis of serum proteins revealed that RNASE1 and MSLN may be potential predictive indicators for the early detection and diagnosis of CAC in SIHD patients. In conclusion, our research extensively examined the variations in serum proteins in patients with SIHD and CAC_SIHD, identifying key indicators and metabolic pathways associated with these conditions. These findings not only provide new insights into the pathological mechanisms of SIHD and CAC_SIHD, but also suggest potential factors for the early diagnosis of CAC in SIHD patients, which imply potential clinical applications.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 2","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10388-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143645492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}