BBA Advances最新文献

{"title":"Deciphering a mechanistic basis for the pathological effect of the GNAO1 E246K variant in neurodevelopmental disorder","authors":"Isra Sadiya ,&nbsp;Irina Nekrasova ,&nbsp;Meirav Avital-Shacham ,&nbsp;Naomi van Wijk ,&nbsp;Keren Zohar ,&nbsp;Nir Kalisman ,&nbsp;Dina Shneidman-Duhovny ,&nbsp;Ehud Banne ,&nbsp;Andreea Nissenkorn ,&nbsp;Lubov Blumkin ,&nbsp;Michal Linial ,&nbsp;Mickey Kosloff","doi":"10.1016/j.bbadva.2026.100182","DOIUrl":"10.1016/j.bbadva.2026.100182","url":null,"abstract":"<div><div>Pathogenic variants in the GNAO1 gene, which encodes for Gα_o, a major neuronal G protein, are associated with neurodevelopmental disorders, epilepsy, and movement disorders. We identified and characterized in detail a de novo heterozygous GNAO1 E246K pathogenic variant in an Israeli female infant with complex developmental delay and substantial motor difficulties. This variant has been reported in other cases as a recurrent pathogenic variant in patients with motor dysfunction and a broad range of neurological outcomes. To investigate the molecular and functional consequences of the Gα_o E246K variant, we employed structural modeling and analysis, mass spectrometry-based proteomics, biochemical assays, and cellular functional assays. Our biochemical results show that this variant does not affect nucleotide binding, nor basal or RGS-accelerated GTP hydrolysis. Despite the E246 position location within a predicted effector binding region, mass spectrometry analysis did not identify any novel cellular partners. Instead, we demonstrate that the E246K variant disrupts the Gα_o regulatory GTPase cycle by directly impairing Gβγ dissociation. This impairment overrides the function of wild-type Gα_o, explaining the dominant effect and the severity of the neurogenetic phenotype despite a heterozygous background. These findings establish a new molecular mechanism for a GNAO1 variant with dominant-negative effects on the GTPase regulatory cycle. The insights gained from studying this mechanism of action provide a basis for developing specific and personalized therapeutic strategies based on the outcome of a missense mutation in GNAO1.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100182"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Collateral lethality of NAD kinase in 1p36 deleted tumors drives vulnerability to NAD kinase 2 depletion","authors":"Saki Suyama-Banjo,&nbsp;Kengo Watanabe,&nbsp;Hirokazu Ishikawa,&nbsp;Yohei Yoshihama,&nbsp;Yasuhide Hirota,&nbsp;Shinji Tsutsumi","doi":"10.1016/j.bbadva.2026.100192","DOIUrl":"10.1016/j.bbadva.2026.100192","url":null,"abstract":"<div><div>The deletion of tumor suppressor genes often occurs in a tumor-specific manner and is accompanied by the unintended loss of adjacent genes. Nicotinamide adenine dinucleotide kinase (<em>NADK</em>), located at a tumor suppressive locus on chromosome 1p36, plays a pivotal role in the biosynthesis of NADP and NADPH and has a closely related paralog, <em>NADK2</em>, in human cells. Although synthetic lethality between NAD kinases was reported in yeast, the relationship between <em>NADK</em> and <em>NADK2</em> in human cells remains unclear. Here, we investigated alterations of the <em>NADK</em> gene expression across various tumor types and assessed whether there is a synthetic lethal relationship between these NAD kinases in human cells. Analysis of The Cancer Genome Atlas dataset revealed <em>NADK</em> gene deletion in multiple tumor types. Depletion of both <em>NADK</em> and <em>NADK2</em> using siRNA decreased cellular NADP(H) levels and inhibited cell proliferation, resulting in the induction of apoptosis. Notably, <em>NADK2</em> knockdown alone markedly impaired cell proliferation and NADP(H) production in <em>NADK</em> homozygous-deleted tumor cells, and also reduced proliferation in <em>NADK</em> heterozygous-deleted tumor cells, whereas in <em>NADK</em>-intact tumor cells only de novo NADP synthesis, but not its intracellular levels or proliferation, was affected. These findings suggest that loss of the <em>NADK</em> gene in tumor cells confers vulnerability to <em>NADK2</em> depletion.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100192"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147802422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MRPL12 regulates high glucose-induced ferroptosis in renal tubular epithelial cells via GPX4","authors":"Guoying Xia,&nbsp;Weiwei Zhang,&nbsp;Jinshi Liu,&nbsp;Jian Yang,&nbsp;Qiuyao Jiang,&nbsp;Wei Xin","doi":"10.1016/j.bbadva.2026.100197","DOIUrl":"10.1016/j.bbadva.2026.100197","url":null,"abstract":"<div><div>Diabetic kidney disease (DKD) is a severe chronic complication of diabetes and one of the major causes of end-stage renal disease (ESRD). Increasing evidence implicates ferroptosis in pathological cell death associated with metabolic diseases, carcinogenesis, and ischemia-reperfusion injury, which is also thought to be involved in kidney tubular cell death under diabetic conditions; however, the underlying pathogenic mechanism remains unclear. We found increased iron level and cellular lipid peroxidation in streptozotocin (STZ)-induced DKD mice and high glucose-stimulated renal tubular cells, accompanied by mitochondrial morphological and functional damages. Further research showed that the expression of mitochondrial ribosomal protein L12 (MRPL12) was downregulated in high glucose conditions. Overexpression of MRPL12 alleviated the damages caused by high glucose-induced ferroptosis in renal tubular cells. MRPL12 interacts with murine double minute 2 (MDM2), an E3 ubiquitin-protein ligase involved in the ubiquitination degradation pathway of several proteins. MRPL12 plays a crucial regulatory role in high glucose-induced ferroptosis of renal tubular epithelial cells by modulating glutathione peroxidase 4 (GPX4), which is a potential novel therapeutic target in improving mitochondrial homeostasis and promoting renal function.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"10 ","pages":"Article 100197"},"PeriodicalIF":4.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13351436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148425023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-stranded nucleic acid binding enhances the in vitro catalytic activity of Chikungunya virus nsP2 protease","authors":"Mohammadamin Mastalipour,&nbsp;Danilo Silva Olivier,&nbsp;Mônika Apareçida Coronado,&nbsp;Andrew J. Dingley,&nbsp;Ruth Anasthasia Siahaan,&nbsp;Alissa Drees,&nbsp;Christian Ahlers,&nbsp;Markus Fischer,&nbsp;Dieter Willbold,&nbsp;Raphael Josef Eberle","doi":"10.1016/j.bbadva.2026.100198","DOIUrl":"10.1016/j.bbadva.2026.100198","url":null,"abstract":"<div><div>Chikungunya virus (CHIKV) is an emerging arbovirus whose replication relies on the multifunctional nonstructural protein 2 (nsP2), particularly its viral protease (nsP2^pro), which is essential for polyprotein processing. In this study, we investigated how interactions with nucleic acids influence nsP2^pro activity. Using High-Throughput Sequencing–Fluorescent Ligand Interaction Profiling (HiTS-FLIP), we identified specific single-stranded DNA aptamers that enhanced nsP2^pro activity. Additionally, both random single-stranded DNA and single-stranded RNA were found to stimulate protease activity, whereas double-stranded DNA showed no such effect. Circular dichroism spectroscopy and secondary structure predictions confirmed that the identified aptamers adopt stable folded conformations. Similarly, structured RNA sequences were also capable of promoting protease activity. The observed stimulatory effect depended on the nucleic acid strand type, length, and buffer conditions, suggesting the involvement of electrostatic interactions. NMR experiments demonstrated that nsP2^pro interacts with single-stranded DNA, accompanied by changes in its conformational dynamics upon binding. Molecular dynamic simulations of nsP2^pro-RNA and -DNA complexes revealed that these nucleic acids interact specifically with the nsP2^pro methyltransferase domain and induce an opening process in the protease active site. Our findings provide novel insights into the regulation of nsP2^pro, enhancing our understanding of CHIKV replication mechanisms, and may guide future antiviral development strategies.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"10 ","pages":"Article 100198"},"PeriodicalIF":4.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13383954/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148608310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hidden faces of alpha-synuclein: Cryo-EM revelation of fibril polymorphs driven by disease, mutations, and PTMs","authors":"Mitra Pirhaghi ,&nbsp;Fatemeh Mamashli ,&nbsp;Bagher Davaeil ,&nbsp;Mahya Mohammad-Zaheri ,&nbsp;Zahra Mousavi-Jarrahi ,&nbsp;Jörg Tatzelt ,&nbsp;Ali Akbar Saboury","doi":"10.1016/j.bbadva.2025.100179","DOIUrl":"10.1016/j.bbadva.2025.100179","url":null,"abstract":"<div><div>Alpha-synuclein (α-Syn) is a neuronal protein implicated in the pathogenesis of several neurodegenerative disorders collectively known as synucleinopathies, including Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy. This article provides a comprehensive overview of the structural characteristics of α-Syn, emphasizing its fibrillar aggregation and the resulting polymorphic fibril forms. Using advances in cryo-electron microscopy, a diverse range of α-Syn fibril polymorphs has been elucidated, both from <em>in vitro</em> preparations and patient-derived brain samples. We further explore the impact of mutation and post-translational modifications—such as truncation and phosphorylation —on α-Syn structure and the unique polymorphs they induce. The article underscores the biological and pathological relevance of α-Syn polymorphism, highlighting how different structural strains may underlie the structural and pathological heterogeneity observed in synucleinopathies. Understanding the mechanisms driving polymorph formation is critical for deciphering disease progression and developing targeted therapeutic strategies.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100179"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGF-β2/OPTN/FOXC1/miR-200 axis regulates actin dynamics in human trabecular meshwork cells","authors":"Chenna Kesavulu Sugali ,&nbsp;Navya Naidu Gajula ,&nbsp;Suresh Chava ,&nbsp;Aramati Bindu Madhava Reddy","doi":"10.1016/j.bbadva.2025.100177","DOIUrl":"10.1016/j.bbadva.2025.100177","url":null,"abstract":"<div><div>Glaucoma is the second leading cause of irreversible blindness globally, with elevated intraocular pressure (IOP) being its primary risk factor. Current therapeutic approaches, such as beta-blockers, alpha-adrenergic agonists, Rho-kinase inhibitors, etc., aim to reduce IOP levels. However, the molecular mechanisms underlying altered IOP remain poorly understood. In this study, we have treated primary human trabecular meshwork cells (HTM) with exogenous dexamethasone (dex) or transforming growth factor beta-2 (TGF-β2) to investigate their effects on glaucoma candidate genes. Interestingly, our findings reveal that FOXC1 acts as a repressor of <em>CYP1B1</em>, and optineurin (OPTN) facilitates the ubiquitination of FOXC1, thereby inducing the expression of CYP1B1. Furthermore, we found that the <em>miR-200</em> family and other miRNAs regulate these glaucoma candidate genes. Furthermore, TGF-β2 downregulates the <em>miR-200</em> family, whereas the <em>miR-200</em> family targets <em>FOXC1</em>, exerting reversible effects by altering the extracellular matrix. Thus, modulating the TGF-β2/OPTN/FOXC1/<em>miR-200</em> axis appears critical in regulating actin dynamics in the anterior eye segment.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100177"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145798104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial convergence of ferroptosis and cuproptosis in castration-resistant prostate cancer: From metabolic vulnerabilities to therapeutic targeting","authors":"Can-lin Wang,&nbsp;Jin-ting Lv,&nbsp;Si-jia Liu,&nbsp;Yang-yang Zhang,&nbsp;Shu-li Wang,&nbsp;Shu-qi Song","doi":"10.1016/j.bbadva.2026.100199","DOIUrl":"10.1016/j.bbadva.2026.100199","url":null,"abstract":"<div><div>Castration-resistant prostate cancer (CRPC) represents the lethal stage of prostate cancer progression and is characterized by persistent therapeutic adaptation, androgen receptor (AR) signaling rewiring, and profound metabolic reprogramming. In recent years, ferroptosis and cuproptosis, two forms of metal-dependent regulated cell death, have emerged as potentially important therapeutic vulnerabilities in CRPC. Ferroptosis is primarily driven by iron-dependent lipid peroxidation, whereas cuproptosis is characterized by copper-induced proteotoxic stress of mitochondrial lipoylated proteins and consequent metabolic collapse. Although these two cell death modalities are mechanistically distinct, accumulating evidence suggests that mitochondria may serve as a critical point of convergence linking them. Mitochondrial metabolic dependency, iron–sulfur cluster homeostasis, lipoylation pathways, membrane organization, and mitochondrial quality control networks collectively shape the susceptibility of CRPC cells to ferroptosis and cuproptosis. In this review, we summarize the mitochondrial basis of ferroptosis and cuproptosis in CRPC and propose that their relationship is better understood as a shared mitochondrial vulnerability architecture rather than as an identical terminal execution pathway. Furthermore, we discuss how mitochondrial metal-death vulnerability may represent a therapeutically exploitable architecture in CRPC, providing a rationale for combination strategies that target ferroptosis, cuproptosis, and mitochondrial metabolic dependency.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"10 ","pages":"Article 100199"},"PeriodicalIF":4.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148738789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of sulfated sialic acids by liquid chromatography coupled with high-resolution mass spectrometry and fluorescence detection","authors":"Sota Yamashita,&nbsp;Takayuki Omoto,&nbsp;Nao Yamakawa,&nbsp;Naoko Komura,&nbsp;Hiromune Ando,&nbsp;Di Wu,&nbsp;Ken Kitajima,&nbsp;Masaya Hane,&nbsp;Chihiro Sato","doi":"10.1016/j.bbadva.2026.100203","DOIUrl":"10.1016/j.bbadva.2026.100203","url":null,"abstract":"<div><div>Sialic acid is localized at the outermost glycan, and involved in regulatory roles as one of the most important glycotopes in various biological phenomena. Recently, we established a highly sensitive and selective method for the fine differentiation of 1,2-diamine-4,5-methylenedioxybenzene (DMB)-labeled sialic acids, including <em>N</em>-acetylneuraminic acid (Neu5Ac), <em>N</em>-glycolylneuraminic acid (Neu5Gc), deaminoneuraminic acid (Kdn), and their <em>O</em>-acetyl derivatives. This approach enables unambiguous identification of these three sialic acids based on characteristic C-5 diagnostic fragment ions obtained by high-resolution accurate-mass spectrometry and fluorescence detection. In the present study, we extended this analytical platform to sulfated sialic acids (SiaSs) to evaluate its applicability to sialic acids bearing an additional negatively charged sulfate group. We first assessed the liquid chromatographic separation of DMB-labeled SiaSs using authentic standards. Using a CAPCELL PAK ADME column, we successfully separated six authentic SiaS standards and three previously unreported SiaS species in sea urchins. We identified multiple <em>O</em>-sulfated substitutions on Neu5Ac and Neu5Gc species, which were further confirmed by characteristic collision-induced dissociation (CID) fragmentation. In addition, electron-activated dissociation (EAD) was employed to evaluate the fragmentation behavior of SiaS species. EAD analyses efficiently generated characteristic diagnostic ions that enable reliable discrimination of the sulfation site, allowing clear differentiation between 8-<em>O</em>- and 9-<em>O</em>-sulfated isomers. Liquid chromatography-based fragment analysis led to the identification of a novel <em>O</em>-sulfated and <em>O</em>-acetylated sialic acid, Neu5Gc8SOAc1, which had never been reported before. These findings underscore the complementary nature of fluorescence detection and high-resolution mass spectrometry techniques for the identification and quantification of DMB-labeled sialic acids.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"10 ","pages":"Article 100203"},"PeriodicalIF":4.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149050717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lysosomal membrane permeabilization is involved in CYP2E1-induced apoptosis in hepatocellular carcinoma cells","authors":"Xuan Wang ,&nbsp;An Wang ,&nbsp;Huanhuan He ,&nbsp;Jiaqi Qiao ,&nbsp;Chengyi Wang ,&nbsp;Haiyuan Du ,&nbsp;Xiji Shu ,&nbsp;Binlian Sun ,&nbsp;Xiaoqing Chen ,&nbsp;Qiongxia Chen ,&nbsp;Xuan Huang ,&nbsp;Shaobo Hu ,&nbsp;Yuchen Liu ,&nbsp;Zhengqi Fu","doi":"10.1016/j.bbadva.2026.100194","DOIUrl":"10.1016/j.bbadva.2026.100194","url":null,"abstract":"<div><div>CYP2E1 expression is often negatively correlated with hepatocellular carcinoma (HCC) progression, and its overexpression induces apoptosis in HCC cells. However, the underlying mechanism of CYP2E1 in apoptosis induction remains unclear. Given the crucial role of lysosomal dysfunction through lysosomal membrane permeabilization (LMP) in promoting apoptosis, this study aimed to investigate whether and how lysosomal dysfunction and LMP contribute to CYP2E1-induced apoptosis in HCC. Here, we demonstrated that CYP2E1 overexpression induced LMP, leading to the translocation of cathepsin D and subsequent apoptosis in HCC cells. Notably, cathepsin D inhibitor attenuated CYP2E1 overexpression-induced LMP and apoptosis. In addition, through sialidase Neuraminidase 4 (NEU4), CYP2E1 overexpression resulted in the deglycosylation and degradation of lysosome-associated membrane protein 1 and 2 (LAMP1/2), contributing to LMP and apoptosis both <em>in vitro</em> and <em>in vivo</em>. Clinically, decreased CYP2E1 expression in the tumor tissues of HCC patients is strongly associated with upregulated LAMP1/2 expression and glycosylation. Collectively, our findings elucidate the role of LMP in CYP2E1-induced cell apoptosis with the involvement of NEU4, providing novel insight for CYP2E1 function in apoptosis.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100194"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147995607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Three-dimensional PCL/collagen electrospun scaffolds with enlarged pores promote cell infiltration for vascular tissue engineering","authors":"Xiaoxuan Zhu,&nbsp;Huiling Lin,&nbsp;Yuxin Li,&nbsp;Yan Yang,&nbsp;Yingxin Chang,&nbsp;Xiong Guo,&nbsp;Mingshi Yang","doi":"10.1016/j.bbadva.2026.100204","DOIUrl":"10.1016/j.bbadva.2026.100204","url":null,"abstract":"<div><div>Cardiovascular disease remains one of the leading threats to human health. Owing to the limited availability of autologous vessels, the demand for vascular graft substitutes continues to rise. The design of tissue-engineered scaffolds that mimic the composition and architecture of the extracellular matrix (ECM) and facilitate vascular remodeling has become a major research focus in artificial blood vessel development. In this study, we investigated how the surface chemical and physical properties of vascular scaffolds influence cellular behavior. Polycaprolactone/collagen (PCL/Col) composite scaffolds were fabricated via electrospinning. The results demonstrated that the hydrophilic/hydrophobic characteristics of the fiber surface significantly affected cell adhesion and proliferation, with collagen incorporation markedly reducing the inherent hydrophobicity of PCL. In addition to chemical properties, the physical topographical cues were also evaluated. To overcome the small pore size typically associated with electrospun membranes, a three-dimensional PCL/Col fibrous scaffold was successfully constructed using a sodium borohydride gas-foaming method. This gas-foaming technique proved to be a simple and efficient approach to enlarging the pore size, thereby promoting cell infiltration, and holds promise as a practical method for preparing vascular basal layer scaffolds.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"10 ","pages":"Article 100204"},"PeriodicalIF":4.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149159033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}