Cell Biochemistry and Function最新文献

{"title":"GRWD1 as a Novel Signature and It Down Regulates IFN in Skin Aging","authors":"Fei Tan,&nbsp;Yaoqun Wang,&nbsp;Peng Xu,&nbsp;Yunjin Li,&nbsp;Yichen Yan,&nbsp;Yutong Gao,&nbsp;Xiaoping Hu,&nbsp;Mengyuan Shen,&nbsp;Qixia Wang,&nbsp;Juan Wang","doi":"10.1002/cbf.70258","DOIUrl":"10.1002/cbf.70258","url":null,"abstract":"<div>\u0000 \u0000 <p>Deep mining of the molecular mechanisms underlying skin aging is critical for the development of novel therapeutic targets. The aim of this study was to explore potential key signatures and underlying mechanisms in skin aging. Bioinformatics tools were used to evaluate the differentially expressed genes (DEGs), perform enrichment analysis, and construct protein-protein interaction networks on datasets. The hub genes were identified using Cytoscape software and then confirmed by qRT-PCR and Western Blot in vitro. We focused on the possible roles of GRWD1. GRWD1 expression were suppressed in senescence model of HDF. After GRWD1 overexpression by lentivirus in primary human dermal Fibroblasts (HDF), transcriptome sequencing (RNA-seq) was performed. GRWD1 has influence on the inflammation and immune responses. IFN signaling pathway genes significant increase in senescence HDF. When GRWD1 overexpressed, decreased expression of IFN pathway is validated. Besides, age-related markers p16, IL-6, and IL-8 expression decreased and Lamin<span>B</span> expression also increased. It was also proved after GRWD1 knockdown. GRWD1 was identified as a novel signature in skin aging. GRWD1 directly interact with IRF3. GRWD1 overexpression can down regulate IFN signaling pathway key genes expression, further diminish IFN aging-inducing effects. GRWD1 alleviates skin inflammatory responses by suppressing IRF3-mediated IFN pathway activation. Our findings suggest that GRWD1 may serve as a molecular biomarker and further as a potential therapeutic target for skin aging.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Japanese Encephalitis Virus and Host Innate Immunity: Insights Into TLR Signaling, PRR Crosstalk, and Viral Immune Evasion","authors":"Mohammad Enamul Hoque Kayesh,&nbsp;Michinori Kohara,&nbsp;Kyoko Tsukiyama-Kohara","doi":"10.1002/cbf.70259","DOIUrl":"10.1002/cbf.70259","url":null,"abstract":"<p>Japanese encephalitis virus (JEV), a neurotropic flavivirus and a major cause of viral encephalitis, poses a significant global health threat due to its neuroinvasive potential. Host innate immune responses, particularly those mediated by pattern-recognition receptors such as Toll-like receptors (TLRs) and RIG-I–like receptors, play critical roles in detecting JEV infection in neurons and glial cells, triggering antiviral defenses through induction of type I interferons (IFNs), inflammatory cytokines, and interferon-stimulated genes. However, dysregulated inflammatory responses may contribute to neurodegeneration and disease severity. JEV has evolved multiple immune evasion strategies, including suppression of IFN signaling, modulation of host microRNAs, and exploitation of cellular pathways such as autophagy to facilitate viral replication and persistence. This review summarizes current knowledge regarding TLR and other PRRs-mediated innate immune sensing during JEV infection, highlights the molecular mechanisms underlying viral immune evasion, and discusses the potential of TLR agonists as antiviral immunomodulators and vaccine adjuvants.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70259","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of PRKCB, NLRC4, and TNFSF10 as Key Regulators of the Lipid Metabolism-Autophagy Network in Atherosclerosis","authors":"Min Li,&nbsp;Yanjun Sun,&nbsp;Yanyi Sun,&nbsp;Zhenyue Chen","doi":"10.1002/cbf.70221","DOIUrl":"10.1002/cbf.70221","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The occurrence and development of atherosclerosis (AS) are closely related to disorders of lipid metabolism and dysfunction of autophagy. However, the key regulatory genes and immune microenvironment characteristics require further exploration.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This study integrated the bulk transcriptome and single-cell RNA sequencing data, and utilized bioinformatics methods to screen the differentially expressed genes (DEGs) of AS. The weighted gene co-expression network analysis (WGCNA) was used to identify the key gene modules related to lipid metabolism and autophagy. The core regulatory genes were further screened based on the machine learning algorithm (LASSO regression). The enrichment scores of 28 immune cell subtypes were calculated by ssGSEA, and the correlation between the immune infiltration characteristics and the expression levels of the three core genes (PRKCB, NLRC4, and TNFSF10) was analyzed by Spearman correlation analysis. The single-cell transcriptome data analysis was performed to determine the cell subtype distribution characteristics of the core genes and to compare the expression differences in lipid metabolism-autophagy-related gene expression across distinct cell subtypes. In addition, we screened potential drugs targeting the key genes from the public drug database, and simulated the binding mode of approved drugs with the active site of PRKCB by molecular docking technology. Ultimately, the expression of target factors in mouse aortic tissues was determined by quantitative real-time PCR (RT-qPCR), Western blotting, and immunohistochemical (IHC) analysis. Concurrently, the levels of TNFSF10 in mouse plasma were confirmed through enzyme-linked immunosorbent assay (ELISA).&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Result&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Three lipid metabolism-autophagy core regulatory genes, PRKCB, NLRC4, and TNFSF10, were identified. These genes were significantly associated with the immune microenvironment of AS plaques and exhibited different cell subpopulation distribution patterns. The macrophage subpopulations showed higher lipid metabolism-autophagy regulatory activity. Molecular docking revealed that the anti-atherosclerotic drugs quercetin and atenolol can stably bind to the active site of PRKCB (with docking energies of -8.3 kcal/mol and -6.2 kcal/mol, respectively), a finding that identifies PRKCB as a candidate target worthy of further attention. Experimental evidence confirmed that the expression of these three key factors was significantly elevated in atherosclerotic plaque tissue, and the levels of TNFSF10 in the plasma of atherosclerotic mice were also signi","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70221","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox Metabolism and Metabolic Vulnerabilities in Diabetes-Driven Pancreatic Cancer: Targeting System Xc−, mTORC1, and Disulfidptosis as Therapeutic Strategy","authors":"Francis Jegan Raj,&nbsp;Anish Ruban Solomonraj,&nbsp;Parimelazhagan Thangaraj","doi":"10.1002/cbf.70249","DOIUrl":"10.1002/cbf.70249","url":null,"abstract":"<div>\u0000 \u0000 <p>Type 2 diabetes mellitus (T2DM) is increasingly recognized as a significant risk factor for pancreatic cancer, with both diseases sharing complex metabolic and molecular underpinnings. Insulin resistance, chronic inflammation, and aberrant activation of the KRAS–mTORC1 signaling axis collectively foster a tumor-permissive microenvironment and disrupt glucose regulation. Recent advances have highlighted disulfidptosis, a novel NADPH-depletion and disulfide-accumulation–driven cell death, as a therapeutic vulnerability in KRAS-mutated, cystine-dependent tumors. This process is linked to the metabolic interplay between glutamate/glutamine and cystine/cysteine, intersecting with mTORC1 signaling and GPX4 regulation. Key regulators, including system Xc⁻, GPX4, and GLUT, orchestrate the interplay between insulin resistance, redox imbalance, and oncogenic signaling in T2DM-associated pancreatic cancer. High expression of cystine/glutamate antiporters (system Xc⁻) promotes cystine accumulation and NADPH depletion, sensitizing tumor cells to disulfidptosis under glucose deprivation. Biomarker-guided precision medicine approaches leverage SLC7A11, GPX4, and p-mTOR expression to identify patient subsets vulnerable to dual metabolic–redox disruption. Emerging therapeutic strategies focus on restricting glucose availability or manipulating antiporters to induce disulfide stress. Integration of metabolic inhibitors with immune checkpoint inhibitors induces immunogenic cell death and overcomes the immunosuppressive pancreatic tumor microenvironment. Targeting these pathways may overcome therapy resistance and improve outcomes in KRAS- or mTOR-driven malignancies. This review synthesizes mechanistic and translational insights into the cyst(e)ine–mTORC1–GPX4 axis, glutaminolysis, biomarker-guided precision medicine, and disulfidptosis, offering a foundation for future therapeutic development in T2DM-associated pancreatic cancer.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of RNA Helicase DHX33 in Tumorigenesis","authors":"Xingshun Wang","doi":"10.1002/cbf.70255","DOIUrl":"https://doi.org/10.1002/cbf.70255","url":null,"abstract":"<div>\u0000 \u0000 <p>RNA helicases are a large family of enzymes crucial for virtually all aspects of RNA metabolism, forming the backbone of gene expression regulation. Among them, DEAH-box helicase 33 (DHX33) has emerged as a pivotal player in fundamental cellular processes, including ribosomal biogenesis, transcription, and translation initiation. A compelling body of evidence now positions DHX33 as a significant oncoprotein, with its overexpression documented in a wide spectrum of human cancers such as lung carcinoma, hepatocellular carcinoma, glioblastoma, and acute myeloid leukemia. Its oncogenic drive is mediated through the transcriptional regulation of genes governing the cell cycle and apoptosis, its interplay with major signaling pathways like Wnt/β-catenin and PI3K/Akt/mTOR, and its role in metabolic reprogramming, notably the Warburg effect. Furthermore, DHX33 acts as a key downstream effector of potent oncogenes like c-Myc. Genetic or pharmacological inhibition of DHX33 consistently impedes tumor growth, underscoring its non-redundant role in oncogenesis. This review systematically synthesizes the current understanding of the mechanisms by which DHX33 promotes tumorigenesis. It delves into its regulation of core cellular processes, its integration into oncogenic signaling networks, and its recently discovered functions in epigenetic and metabolic reprogramming. By consolidating this knowledge, we aim to highlight the multifaceted nature of DHX33 in cancer biology and firmly establish its potential as a viable and promising therapeutic target for future anticancer strategies.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148358020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative Control of Transposable Elements: From Genome Plasticity to Immune Regulatory Circuits","authors":"Irving Jesús Reyes-Barragán","doi":"10.1002/cbf.70252","DOIUrl":"https://doi.org/10.1002/cbf.70252","url":null,"abstract":"<p>Transposable elements (TEs) constitute nearly half of the human genome and are increasingly recognized as context-dependent regulators of genome function rather than passive repetitive DNA. This Review synthesizes classical and recent evidence on TE biology, including TE classification, mechanisms of mobilization, host restriction pathways, insertional mutagenesis, and contributions to gene regulation. We emphasize that TE activity operates across a spectrum: controlled TE expression can contribute cis-regulatory modules, non-coding RNAs, chromatin states, and immune enhancers, whereas excessive or misregulated TE activity can promote genome instability, innate immune activation, and inflammatory pathology. To reduce conceptual redundancy, we organize these processes within an integrative framework, the Transposon Circuitry Theory of Immune Regulation (TACTIR), which links TE-derived modules, chromatin control of TE transcription, stress pathways, and immune gene networks. In this model, TE-derived enhancers and transcription factor motifs may shape stimulus-responsive gene expression, while TE transcripts and reverse-transcribed products can engage innate immune sensors under specific states of derepression. We also discuss how TE-linked regulatory states may contribute to trained immunity and T-cell dysfunction, while distinguishing established mechanisms from inferred or hypothetical links. Clinically, we place TE-mediated insertional disease, cancer-associated TE dysregulation, and immune modulation in appropriate context, noting that TE insertions account for a minority of genetic disease cases but provide important mechanistic examples of genome vulnerability. Finally, we consider how genome-editing approaches and transposon-derived tools can clarify TE function and enable translational applications. Together, this Review frames TEs as regulated genomic elements that connect genome plasticity, immune responsiveness, and disease susceptibility.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70252","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148358080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic Effect of Digoxin and Cisplatin on Redox Imbalance in HeLa Cells.","authors":"Duane Gischewski Pereira, Israel José Pereira Garcia, Graziele Aparecida Silva Maia, Jéssica Martins Moura de Valadares, Ana Carolina Pacheco Ramos, Herica Lima Santos, Silvana Gisele Pegorin de Campos, José Augusto Fp Villar, Leandro A Barbosa, Vanessa Faria Cortes","doi":"10.1002/cbf.70273","DOIUrl":"10.1002/cbf.70273","url":null,"abstract":"<p><p>Our previous study demonstrated a potent synergistic antitumor effect between 1 nM digoxin and 1 μM cisplatin in cervical cancer cells, which was dependent on the modulation of the signaling pathway involving Na, K-ATPase/Src. Because of the relationship between Na, K-ATPase/Src and the modulation of oxidative stress, the aim of this study was to demonstrate the effect of combined treatment with digoxin and cisplatin on oxidative stress parameters in HeLa cells and the effect of treatment in non-tumor cell lines. Analysis of oxidative stress parameters revealed a significant reduction in cellular antioxidant defense mechanisms, SOD activity, and content of reduced total thiol groups. Additionally, there was an increase in H₂O₂ content within 24 h, confirming the elevated cellular oxidative stress during the combined treatment. Furthermore, lipid peroxidation and lipid droplet formation levels were evaluated, showing an increase in these parameters after 48 h of treatment, consistent with oxidative stress. Compared to the other tested cell lines, the combined treatment did not significantly alter cell viability compared to the control. Our data demonstrate that the synergistic antitumor effects of digoxin and cisplatin in HeLa cells are tightly associated with increased oxidative stress via activation of the Na, K-ATPase/Src/ROS signaling pathway, may resulting in antiproliferative and pro-apoptotic effects. These findings indicate that oxidative stress is a key component of the cellular response underlying the synergistic antitumor effects of digoxin and cisplatin.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":"e70273"},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13408207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral Calcium Supplements With L-Proline and Sodium Zinc Chlorophyllin Preserve Elevated Transepithelial Calcium Transport in Spontaneously Hypertensive Rats","authors":"Pornpailin Upanan,&nbsp;Kannikar Wongdee,&nbsp;Surathouch Thongprong,&nbsp;Nithipak Thammayon,&nbsp;Jarinthorn Teerapornpuntakit,&nbsp;Wacharaporn Tiyasatkulkovit,&nbsp;Surachai Chantip,&nbsp;Wasutorn Chankamngoen,&nbsp;Tanapan Siangcham,&nbsp;Waranurin Yisarakun,&nbsp;Nattapon Panupinthu,&nbsp;Sakamon Devahastin,&nbsp;Narattaphol Charoenphandhu","doi":"10.1002/cbf.70256","DOIUrl":"https://doi.org/10.1002/cbf.70256","url":null,"abstract":"<div>\u0000 \u0000 <p>Hypertensive rodents often exhibit bone loss and osteopenia with impaired bone formation. We hypothesized that spontaneously hypertensive rats (SHR) could compensate for osteopathy through certain mechanisms, particularly intestinal calcium absorption. However, this calcium transport may be suppressed after long-term exposure to high luminal calcium levels during calcium supplementation through a molecular mechanism known as calcium-dependent inactivation of calcium channels. Herein, we designed calcium-rich formulations—that is, 14 mM CaCl₂ + 12 mM <span>l</span>-Proline +20 µM sodium zinc chlorophyllin (CaA) and 14 mM CaCl₂ + 12 mM <span>l</span>-Proline +60 µM sodium zinc chlorophyllin (CaB), with a total elemental calcium amount of &lt; 16 mg/kg/day—administered orally to SHR and wild-type rats (WT), aiming to avoid suppressing the calcium transport rate. We found that SHR had greater systolic, diastolic, and mean arterial pressures than WT, while both CaA and CaB did not alter these parameters. Using an Ussing chamber with ⁴⁵Ca radioactive tracer, both regimens did not affect the enhanced transepithelial calcium transport in the duodenum of SHR, although they increased epithelial potential difference and short-circuit current, indicators of electrogenic ion fluxes. Meanwhile, they did not alter mRNA expression levels of calcium transporters or tight junction components in the mucosal cells. In conclusion, unlike the known suppressive effects of certain calcium compounds on calcium absorption, oral administration using CaA and CaB formulations maintained high transport rates in SHR. This finding helps provide a basis for further clinical investigation into the optimization of calcium supplementation, particularly in the context of hypertension and osteoporosis.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148357959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal MicroRNA-424-5p From Polycystic Ovary Syndrome Follicular Fluid Attenuates Ovarian Inflammation via Targeting the Fibroblast Growth Factor 2/Fibroblast Growth Factor Receptor 1 Axis","authors":"Dong Yuan,&nbsp;Xiaoming Hao,&nbsp;Jing Luo,&nbsp;Yi Liu,&nbsp;Pingjie Du,&nbsp;Zhu Yang","doi":"10.1002/cbf.70248","DOIUrl":"https://doi.org/10.1002/cbf.70248","url":null,"abstract":"<div>\u0000 \u0000 <p>Sustained low-grade inflammation is increasingly recognized as a central element in how polycystic ovary syndrome (PCOS) develops. Here we set out to clarify what role follicular fluid (FF)-borne exosomal miR-424-5p plays in shaping ovarian inflammation and how this ties in with the ovulatory problems seen in PCOS. Across FF samples taken from patients, miR-424-5p levels tracked inversely with pro-inflammatory cytokine concentrations to a striking degree. When granulosa cells (GCs) were challenged with lipopolysaccharide (LPS), delivering exosomal miR-424-5p dampened cytokine release and restored the expression of ovulation-linked genes. Using a dual-luciferase reporter assay, we traced this effect to FGF2, which miR-424-5p binds directly, and we found FGF2/FGFR1 signaling to be conspicuously raised in PCOS. In dehydroepiandrosterone (DHEA)-treated rats modeling the syndrome, giving exosomal miR-424-5p eased ovarian inflammation and brought back part of the lost ovulatory capacity. Taken together, the data suggest that exosomal miR-424-5p tempers ovarian inflammation in PCOS by holding the FGF2/FGFR1 axis in check, which casts fresh light on the follicular abnormalities that mark this condition.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148357971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxicity of Organic Acids Leading to Renal Dysfunction in Glutaric Acidemia Type I: A Mini Review","authors":"Luísa Tedesco,&nbsp;Gillian Guerreiro,&nbsp;Bianca Gomes dos Reis,&nbsp;Franciele Fátima Lopes,&nbsp;Debora Tonelotto,&nbsp;Luiza Wailer,&nbsp;Ana Kalise Böttcher,&nbsp;Marina Acosta,&nbsp;Carmen Regla Vargas","doi":"10.1002/cbf.70253","DOIUrl":"https://doi.org/10.1002/cbf.70253","url":null,"abstract":"<div>\u0000 \u0000 <p>Glutaric Acidemia type I is an inborn error of metabolism that impairs the metabolism of lysine, hydroxylysine, and tryptophan, leading to neurologic and, as more recently described, acute and chronic kidney damage. This mini review explores the available literature regarding renal impairment in GA-1 and highlights the possible mechanisms involved. Most case reports regarding patients presenting acute kidney dysfunction indicate the tubules as the main site of impairment, which was also found in the animal model for this disease, especially under metabolic decompensation. In addition to that, a mild progressive decline in glomerular filtration rates has been found in GA-1 patients, independently of treatment quality and neurologic outcomes. Taken together, such findings reveal the importance of further investigation on the association between GA-1 and kidney function, encompassing the need for adequate therapeutic approaches and biomarkers that target these alterations.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148358182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}