Biochimica et biophysica acta. Molecular basis of disease最新文献

{"title":"Depression- and exercise-associated stimuli exert contrasting effects on neural stem cell activity and paracrine signaling","authors":"André L. Simão ,&nbsp;Sónia Sá Santos ,&nbsp;João A. Ferreira Moreira ,&nbsp;Francisca Silva ,&nbsp;Raúl Oliveira ,&nbsp;Catarina Roxo ,&nbsp;Matilde Santos ,&nbsp;Ana Rita Vaz ,&nbsp;Dora Brites ,&nbsp;Margarida F.B. Silva ,&nbsp;Sandra H. Vaz ,&nbsp;Rui S. Rodrigues ,&nbsp;João B. Moreira ,&nbsp;Joana M. Mateus ,&nbsp;Ana M. Sebastião ,&nbsp;Rui E. Castro ,&nbsp;Sara Xapelli ,&nbsp;Susana Solá","doi":"10.1016/j.bbadis.2025.167997","DOIUrl":"10.1016/j.bbadis.2025.167997","url":null,"abstract":"<div><div>Adult neurogenesis is dysregulated in neurological disorders, including depression. Adult neural stem cells (NSCs) are close to the vasculature and the cerebrospinal fluid, placing them in an ideal position to receive extrinsic signals and transmit these cues to the neurogenic niche. Herein, we aimed to explore how different systemic cues influence the regenerative properties of NSC secretome on recipient differentiating cells and microglia, key neurogenic components. To mimic signals that NSCs may sense in pathological conditions, we used the secretome of oxidative damaged cells (acute oxidative damage), and the serum from depressed mice (depression-associated chronic signals). Alternatively, NSCs were conditioned with different mitochondrial metabolic regulators to mimic a pro-metabolic NSC environment. Results showed that both injury and metabolic stimuli triggered the increase of NSC proliferation and mitochondrial fragmentation, along with the delivery of a neuroprotective secretome toward injured recipient cells. However, premature differentiation was only observed in NSCs sensing depression-associated chronic signals. The secretome from metabolic-stimulated NSCs favored neurogenesis of target cells, being enriched in regenerative metabolites. Depression-associated signals promoted a NSC secretome with reduced regenerative metabolites and microRNAs that repressed microglial phagocytosis and differentiation in target NSCs. At last, the reduction of oxidative phosphorylation-related proteins in the neurogenic niche of depressed mice was rescued by physical exercise. Our data indicate a central role of external metabolic and injury signals in regulating the neurogenic niche through NSC paracrine activity, unveiling distinct NSC regenerative responses upon transient acute and chronic injuries, and new cues for physical exercise-induced alleviation of depression.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167997"},"PeriodicalIF":4.2,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144738209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRAG1 promotes cholangiocyte epithelial-mesenchymal transition and liver fibrosis in biliary atresia","authors":"Wei Zhu ,&nbsp;Zhongxian Zhu ,&nbsp;Jie Feng ,&nbsp;Yao Lu ,&nbsp;Ruyi Zhang ,&nbsp;Zequan Ding ,&nbsp;Hua Xie ,&nbsp;Weibing Tang","doi":"10.1016/j.bbadis.2025.167994","DOIUrl":"10.1016/j.bbadis.2025.167994","url":null,"abstract":"<div><div>Biliary atresia (BA) is a severe pediatric liver disease in which progressive liver fibrosis (LF) significantly affects the prognosis. Epithelial-mesenchymal transition (EMT) is considered a key factor in the development and progression of LF. This study aimed to investigate the role and mechanism of PEAK1-related kinase activating pseudokinase 1 (PRAG1) in the EMT-related LF process in BA. We found that the expression of PRAG1 was significantly elevated in both patients with BA and the bile duct ligation (BDL) model, and predominantly localized on biliary epithelial cells. Also, the expression of PRAG1 positively correlated with the cholangiocyte marker KRT19 and the mesenchymal marker ACTA2, and increased with the severity of fibrosis. In human intrahepatic biliary epithelial cells (HIBECs), PRAG1 promoted the expression of mesenchymal markers (VIM and ACTA2) and fibrosis markers (COL1A1 and FN1), inhibited the expression of the epithelial marker CDH1, and enhanced cell proliferation. The key factor of EMT-SNAIL1 presented increased expression and delayed degradation after overexpression of PRAG1. Moreover, we identified PRAG1 could bind with F-box protein 11 (FBXO11) and subsequently reversed FBXO11-mediated inhibition of SNAIL1 protein expression, cell proliferation, and the EMT phenotype. This study provides the potential role of PRAG1 in the mechanisms underlying the LF progression of BA.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167994"},"PeriodicalIF":4.2,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144724406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dimeric PKM2 induces ferroptosis from intestinal ischemia/reperfusion in mice by histone H4 lysine 12 lactylation-mediated HMGB1 transcription activation through the lactic acid/p300 axis","authors":"Zan Liu ,&nbsp;Yuxiang Zhou ,&nbsp;Ming Li ,&nbsp;Zhenghui Xiao ,&nbsp;Zitong Zhao ,&nbsp;Yong Li","doi":"10.1016/j.bbadis.2025.167998","DOIUrl":"10.1016/j.bbadis.2025.167998","url":null,"abstract":"<div><h3>Background</h3><div>The role of Pyruvate kinase M2 (PKM2) in intestinal ischemia-reperfusion (I/R) was investigated in this study, with a focus on the mechanism of dimeric PKM2 in ferroptosis.</div></div><div><h3>Methods</h3><div>The in vivo and in vitro models of intestinal ischemia-reperfusion were constructed and in vitro and in vivo evaluations were performed using a variety of techniques.</div></div><div><h3>Results</h3><div>HMGB1 and dimeric PKM2 were highly expressed in intestinal I/R mice. Dimeric PKM2 inhibitors (ML265) and HMGB1 inhibitors (Glycyrrhizin) reduced ferroptosis in vivo and in vitro. ML265 decreased glucose uptake, lactate, GLUT1, ENO1, LDHA, and PDK1 levels. Importantly, HMGB1 knockdown completely counterbalanced the promoting effect of PKM2 overexpression on ferroptosis, while ACSL4 knockdown or GPX4 overexpression partially revoked the promoting effect of PKM2 overexpression on ferroptosis. HMGB1 overexpression completely prevented the inhibiting effect of PKM2 knockdown on ferroptosis. Lactate promoted pan kla and H4K12la levels in H/R-induced Caco-2 cells and promoted ferroptosis. ML265 reversed the phenomenon. Moreover, CoIP results showed that PKM2 directly bound to p300. ChIP-qPCR results showed that the concentration of dimeric PKM2 (and nuclear PKM2) and p300 on HMGB1 promoter increased in H/R group. ML265 reduced the enrichment of p300 on HMGB1 promoter. Sh-p300 reduced H4K12la enrichment on HMGB1 promoter. In addition, oe-p300 disrupted the effect of ML265 on H/R-induced Caco-2 cells.</div></div><div><h3>Conclusions</h3><div>Our results suggested that dimeric PKM2 induced ferroptosis in intestinal I/R by stimulating lactylation-mediated HMGB1 transcription activation via the lactic acid/p300 axis, which may provide new targets for treatment of intestinal I/R injury.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167998"},"PeriodicalIF":4.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of conformation-specific antibodies TOMA-1 and TTCM-1 for recombinant tau monomer and amplified brain derived tau oligomer","authors":"Md Anzarul Haque ,&nbsp;Mauro Montalbano ,&nbsp;Sheeza Khan ,&nbsp;Nicha Puangmalai ,&nbsp;Nemil Bhatt ,&nbsp;Nikita Shchankin ,&nbsp;Cynthia Jerez ,&nbsp;Rakez Kayed","doi":"10.1016/j.bbadis.2025.167995","DOIUrl":"10.1016/j.bbadis.2025.167995","url":null,"abstract":"<div><div>Tauopathies are a set of neurodegenerative diseases characterized by the pathological accumulation of aggregated tau in the brain. Recent breakthrough evidence has revealed the existence of different strains of tau oligomer (TauO) which direct the different pathological presentation of individual tauopathies. Extensive research efforts have been devoted to search for specific antibodies or drug candidates which target TauO to serve as promising alternatives to treat Alzheimer's disease (AD) in future. To screen for the antibodies which are able to bind with amplified brain derived tau oligomer (aBDTO), we have investigated the binding parameters of the tau oligomer-specific monoclonal antibody-1 (TOMA-1) and toxic tau conformation-specific monoclonal antibody-1 (TTCM-1) with the recombinant tau monomer (rTauM) and aBDTO using isothermal titration calorimetry (ITC). TOMA-1 specifically recognizes the amino acid sequences 367–386, 382–401 and 367–386 and TTCM-1 specifically recognizes the amino acid sequence 307–326 of rTauM and aBDTO, respectively. Our results demonstrated that both TOMA-1 and TTCM-1 have a high binding affinity with aBDTO compared to rTauM. We also observed that higher the binding affinity of the antibody to the aBDTO, lower was the toxicity of the aBDTO and vice versa. Our study taken together presents both TOMA-1 and TTCM-1 to be potential immunotherapeutic agents against AD.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167995"},"PeriodicalIF":4.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144738210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia facilitates stemness of colon cancer cells via histone lactylation","authors":"Qi Zhang ,&nbsp;Zhenzhen Han ,&nbsp;Jia-Hui Liu ,&nbsp;Munan Li ,&nbsp;Wei Li ,&nbsp;Xin Zhou ,&nbsp;Xuelian Liu","doi":"10.1016/j.bbadis.2025.167993","DOIUrl":"10.1016/j.bbadis.2025.167993","url":null,"abstract":"<div><div>The hypoxic tumor microenvironment, a hallmark of advanced solid tumors, is strongly associated with poor prognosis and reduced survival in colon cancer patients. Emerging evidence indicates that hypoxia serves as a key driver of cancer stemness by promoting the formation and maintenance of cancer stem cells (CSCs). However, the precise molecular mechanisms through which hypoxia induces CSC formation remain incompletely understood, particularly regarding the metabolic-epigenetic regulation of stemness characteristics. This study uncovers histone lactylation as a pivotal metabolic-epigenetic switch linking hypoxic stress to stemness in colorectal cancer cells. We demonstrate that hypoxia activates the HIF-1α/LDHA axis, driving lactate accumulation and triggering global histone lactylation (particularly H3K18la) in HT29 and SW480 cells. Crucially, lactylated histones directly bind and activate stemness gene promoters (<em>OCT4</em>/<em>CD44</em>/<em>c-MYC</em>), correlating with enhanced tumorsphere formation. Mechanistic validation through CRISPR-dCas9-HDAC3-mediated promoter-specific delactylation impaired stemness gene expression, demonstrating lactylation as a causal regulator. Our findings establish histone lactylation as a critical epigenetic regulator of hypoxia-induced stemness in colon cancer, revealing both its fundamental biological role and therapeutic potential. Targeting this lactylation-dependent pathway may disrupt CSC formation and enhance treatment efficacy.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167993"},"PeriodicalIF":4.2,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144736001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The genotype/phenotype conundrum of inherited mitochondrial disorders: Insights from a survey of mtDNA mutations associated with Leigh syndrome in complex I","authors":"Zeinab Alsadat Ahmadi,&nbsp;Ulrich Brandt","doi":"10.1016/j.bbadis.2025.167996","DOIUrl":"10.1016/j.bbadis.2025.167996","url":null,"abstract":"<div><div>Mitochondrial disorders encompass a broad spectrum of genetic disorders impairing mitochondrial function. Considerable advancements have been made in the diagnosis and clinical management of these primary mitochondrial diseases. However, diagnosis and treatment have remained largely empirical, because the pathogenic mechanisms are still poorly understood by which any of the numerous known mutations lead to a specific phenotype in patients. To make inroads into this central challenge of mitochondrial medicine, we performed a focused survey of a cohort of published cases of Leigh syndrome caused by point mutations in subunits of respiratory chain complex I encoded by the mitochondrial genome. Leigh syndrome is one of the most severe mitochondrial disorders and is characterized by clinical and genetic manifestations predominantly affecting the central nervous system and the brain. We found that even basic correlations between a specific molecular defect and disease severity and progression are often obscured by the heterogeneity of the available diagnostic data. Still, our analysis showed that in order to understand the specific pathogenic impact it entails, for each mutation one has to carefully differentiate which functional domain of complex I is actually affected. It seems evident that much more comprehensive and differentiated studies of representative mutations as well as far more complete and standardized diagnostic data from patients should be obtained. This will be prerequisite for understanding and discriminating pathogenic mechanisms as a way to develop effective rational therapies for Leigh syndrome and other mitochondrial disorders.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167996"},"PeriodicalIF":4.2,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144736002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impaired ciliogenesis in small airway epithelial cells involves in the development of idiopathic pulmonary fibrosis","authors":"Zhaoni Wang ,&nbsp;Xiangsheng Yang ,&nbsp;Qingyang Yu ,&nbsp;Xin Xu ,&nbsp;Jianxing He ,&nbsp;Nanshan Zhong ,&nbsp;Xiao Xiao Tang","doi":"10.1016/j.bbadis.2025.167992","DOIUrl":"10.1016/j.bbadis.2025.167992","url":null,"abstract":"<div><div>Accumulating evidence suggests that abnormalities in airway epithelial cells involve in the development of idiopathic pulmonary fibrosis (IPF). However, whether ciliary impairment contributes to IPF pathogenesis is unspecified. In this study, we evaluated the ciliogenesis potency of IPF-derived small airway epithelial cells (SAECs), assessed the effect of aberrant ciliogenesis on lung fibroblast activation and further identified whether improving ciliogenesis could attenuate pulmonary fibrosis. Here, we showed that upon external injury or serial cell passage, IPF-derived SAECs had greater decline in ciliogenesis potency as compared to healthy control (HC). Conditioned medium harvested from SAECs post injury, serial passage or silencing the ciliogenesis regulator <em>FOXJ1</em> promoted the expression of α-smooth muscle actin (α-SMA) and fibronectin (FN) in human lung fibroblasts as compared to their corresponding controls. Mice with bleomycin (BLM)-induced lung fibrosis had reduced number of ciliated cells as compared to the saline control, while overexpressing <em>Foxj1</em> in mouse lung attenuated the extent of pulmonary fibrosis. LY450139, a γ-secretase inhibitor, could also improve ciliogenesis in IPF-derived SAECs and inhibit lung fibroblast activation induced by ciliogenesis impairment. We demonstrated the contributing role of ciliogenesis impairment in IPF pathogenesis. Targeting the ciliogenesis abnormality may be a potential therapeutic strategy for IPF.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167992"},"PeriodicalIF":4.2,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144719202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of eIF5A hypusination as a unique and underexplored mechanism in proteinopathies and neurological diseases","authors":"Rohan Desai ,&nbsp;Daniel C. Lee ,&nbsp;Maj-Linda B. Selenica","doi":"10.1016/j.bbadis.2025.167991","DOIUrl":"10.1016/j.bbadis.2025.167991","url":null,"abstract":"<div><div>Eukaryotic Translation Initiation Factor 5A (eIF5A) undergoes a unique post-translational modification of hypusination, converting a lysine 50 residue to hypusine (hypK50). While a few studies have investigated the role of the spermidine-hypusine-eIF5A axis in neurodegenerative diseases, including the pathological accumulation of tau and TAR DNA-binding protein 43 (TDP-43), the role of the hypusine pathway in neurological diseases remains vastly understudied. Thus, the focus of this review is highlighting emerging research on the mechanisms by which aberrant and chronic increases in hypusinated eIF5A (eIF5A^hypK50) govern nucleocytoplasmic transport, stress granule dynamics, and protein aggregation to encourage further research of this pathway in multi-etiology dementia.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167991"},"PeriodicalIF":4.2,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144710281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KDELR: Beyond protein retrieval, a novel regulator in cancer progression","authors":"Diego Tapia ,&nbsp;Felipe Garín-Ortiz ,&nbsp;Emilia Flores ,&nbsp;Manuel Varas-Godoy ,&nbsp;Alejandro Godoy ,&nbsp;Jorge Cancino","doi":"10.1016/j.bbadis.2025.167981","DOIUrl":"10.1016/j.bbadis.2025.167981","url":null,"abstract":"<div><div>Eukaryotic cells interact with their environment through the secretory pathway, which involves the endoplasmic reticulum (ER), Golgi complex (GC), and endolysosomal system. These organelles regulate protein folding, post-translational modifications, and trafficking of structural and signaling proteins essential for cellular homeostasis. The KDEL receptor (KDELR), a cargo and signaling receptor located in the Golgi complex (GC), plays a crucial role in maintaining the balance of the secretory pathway by sensing cargo arrival from the endoplasmic reticulum (ER) and activating signaling pathways. Dysfunction in this pathway contributes to diseases such as diabetes, neurodegenerative disorders, and cancer. Recent studies highlight KDELR's involvement in cancer progression, yet its precise role remains unclear. This review provides an overview of KDELR's structure and function, highlighting its emerging significance in cancer biology.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167981"},"PeriodicalIF":4.2,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elafin inhibits macrophage activation by blocking a chloride channel","authors":"Xia Li ,&nbsp;Longxin Chen ,&nbsp;Na Chen ,&nbsp;Liang Xu ,&nbsp;Xiaoli Cui ,&nbsp;Feng Wang","doi":"10.1016/j.bbadis.2025.167989","DOIUrl":"10.1016/j.bbadis.2025.167989","url":null,"abstract":"<div><div>The molecular mechanisms underlying the anti-inflammatory functions of elafin, beyond its role as a serine protease inhibitor, have garnered significant interest. In this study, we engineered an antibody-elafin fusion construct (Her-elafin) by grafting elafin into the complementarity-determining region (CDR) of the Herceptin antibody. Her-elafin retained the full inhibitory activity of elafin against neutrophil elastase and effectively suppressed lipopolysaccharide (LPS)-induced macrophage activation. Using Her-elafin as a molecular probe, we identified that elafin specifically binds to and inhibits Clic1, a chloride channel expressed on macrophages. This binding likely reduces intracellular reactive oxygen species (ROS) production, thereby attenuating downstream inflammatory cascades. Furthermore, the dual inhibitory activities of Her-elafin against neutrophil elastase and Clic1 resulted in significant anti-inflammatory effects in a murine model of acute lung injury, highlighting its potential as a promising therapeutic strategy.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 8","pages":"Article 167989"},"PeriodicalIF":4.2,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144676827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}