Biological Research最新文献

{"title":"Coffea arabica pulp aqueous extract exhibits the anti-colitogenic effect in mice: preventive efficacy and possible mechanisms of action.","authors":"Apiwan Arinno, Pichayapa Sukmak, Supisara Treveeravoot, Purit Kulworasreth, Pitsinee Supapol, Withsakorn Sangsuwan, Natnicha Teansuk, Wanapas Wachiradejkul, Jakkapong Inchai, Thaniya Sricharunrat, Kanthida Jangyubol, Patthadon Sanghong, Chutima S Vaddhanaphuti, Chanat Aonbangkhen, Pawin Pongkorpsakol","doi":"10.1186/s40659-026-00696-9","DOIUrl":"10.1186/s40659-026-00696-9","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) is a chronic inflammatory disease caused mainly by immune overactivation and intestinal mucosal barrier disruption. Coffea arabica pulp aqueous extract (CPE) contains a number of bioactive phenolic compounds that exhibit antioxidant and anti-inflammatory effects with previously unexplored application in experimental colitis. The aim of this study is to determine whether CPE produces anti-colitogenic effect and its possible mechanism of action. We found that CPE attenuated all IBD-related phenotypes and increased survival rates in dextran sulfate sodium (DSS)-induced colitis mice. In addition, CPE significantly suppressed mRNA and protein expression of myosin light-chain kinase (MLCK). Furthermore, CPE also inhibited MLCK recruitment to apical junction of colonic tissues of colitis mice. Although CPE had no effect on mRNA expression of tight junction genes, it reversed inflammation-mediated downregulation of ZO-1, occludin, and claudin-4 proteins in colitis mice. Importantly, CPE was able to recover ZO-1 and occludin localization to apical junction and suppressed tight junction-dependent leak pathway permeability in colitis mice. Indeed, CPE was also capable of stimulating sirtuin-1 (SIRT-1) in colonic tissues obtained from DSS-induced colitis mice, which is known to suppress inflammation and enhance intestinal barrier function. Therefore, SIRT-1 has been shown to be associated with CPE treatment in IBD model.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13366971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147980425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockout of filamin A in KGN granulosa tumor cells impairs proliferation, cell cycle progression, migration, and cytoskeletal organization under mechanical stress.","authors":"Yuhao Jiang, Karolina Magdalena Caban, Mirko Peitzsch, Carola Herrmann, Doris Mayr, Jan Bernd Stöckl, Thomas Fröhlich, Artur Mayerhofer, Annette Müller-Taubenberger, Harald Welter","doi":"10.1186/s40659-026-00686-x","DOIUrl":"10.1186/s40659-026-00686-x","url":null,"abstract":"<p><strong>Background: </strong>Filamin A (FLNA) is an actin-binding protein that regulates mechanosensitivity and functions as an intracellular signaling scaffold in various cell types. It has also been implicated in tumor growth. We recently reported FLNA expression in human ovarian granulosa cells and in KGN cells, a granulosa cell tumor (GCT) line.</p><p><strong>Results: </strong>Immunohistochemistry analysis of 51 GCT samples revealed heterogeneous FLNA expression, with approximately 20% showing weak, 18% strong, and the majority moderate expression. We therefore conducted functional studies in KGN cells using CRISPR/Cas9 gene editing. A proteomic approach revealed marked changes in protein abundance upon FLNA depletion: proteins with increased abundance were predominantly related to adhesion, cytoskeletal organization, regulation of cell shape, and lipid metabolic process, whereas those with decreased abundance were associated with DNA replication, cell division, and cell cycle regulation. FLNA-knockout cells showed enlarged cell sizes, reduced proliferation, and slightly affected steroidogenesis. Disruption of FLNA further reduced migration velocity, altered actin cytoskeletal alignment under flow, and modified expression of genes involved in cytoskeletal architecture, adhesion, and mechanosensing under shear stress.</p><p><strong>Conclusions: </strong>Our results identify crucial roles of FLNA in shaping the cellular architecture, motility, and proliferation of KGN cells. Consequently, alterations in FLNA expression may influence intracellular signaling, and responsiveness to mechanical cues in both physiological and pathological contexts.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13200416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147980358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Cisplatin-induced azoospermia and testicular damage ameliorated by adipose-derived mesenchymal stem cells.","authors":"Hamdy Y Ismail, Nora A Shaker, Shaymaa Hussein, Adel Tohamy, Mohamed Fathi, Hamdy Rizk, Y R Wally","doi":"10.1186/s40659-026-00697-8","DOIUrl":"10.1186/s40659-026-00697-8","url":null,"abstract":"","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"59 1","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13169876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147926235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of galectins in modulating the tumor microenvironment and driving metastasis in skin cancers.","authors":"Mohsen Dabagh, Alina Ciceu, Cornel Balta, Maria Consiglia Trotta, Bartolo Ferraro, Giovanbattista D'Amico, Anca Hermenean, Vlad Mihail Voiculescu","doi":"10.1186/s40659-026-00695-w","DOIUrl":"10.1186/s40659-026-00695-w","url":null,"abstract":"<p><p>Galectins, a family of β-galactoside-binding lectins, are key regulators of tumor progression, immune evasion, and therapy resistance in skin cancers. Among them, Galectin-1, Galectin-3, and Galectin-9 have been most extensively investigated for their multifaceted roles in shaping the tumor microenvironment. These proteins influence cancer cell proliferation, apoptosis, angiogenesis, and immune cell responses through both intracellular and extracellular mechanisms. Galectin-1 and Galectin-3 modulate immune checkpoint pathways and cancer-associated fibroblast activation, whereas Galectin-9 interacts with TIM-3 to induce T-cell exhaustion. Other family members, including Galectin-7 and Galectin-8, display context-dependent functions that may either promote or inhibit tumor development. Recent preclinical and early clinical trials targeting galectins, such as the Gal-3 inhibitors belapectin and GB1211, highlight their translational potential as adjuncts to immunotherapy. This review summarizes current knowledge on galectin expression and function in melanoma and non-melanoma skin cancers, emphasizing their contribution to immune escape and therapeutic resistance, as well as challenges and perspectives for galectin-targeted interventions.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147926183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phyllanthus niruri niosomes ameliorate obesity-induced hepatic steatosis in rats via modulating MALAT1/miR-206/GLP-1R signaling and hepatic lipid metabolism.","authors":"Safaa I Khater, Mohamed M A Hussein, Saydat S Abdel-Magied, Marwa M Lotfy, Tarek Khamis, Sahar Abdelaziz, Mahmoud Mostafa, Noha Osama El-Shaer, Mahran Mohamed Abd El-Emam","doi":"10.1186/s40659-026-00682-1","DOIUrl":"10.1186/s40659-026-00682-1","url":null,"abstract":"<p><p>Metabolic dysfunction associated fatty liver disease (MAFLD) is a rapidly growing global health burden characterized by hepatic lipid accumulation, insulin resistance, oxidative stress, and inflammation. Phyllanthus niruri (PHYLN) is rich in polyphenols and lignans with known antioxidant and anti-inflammatory properties; however, its therapeutic efficacy is limited by poor bioavailability. This study investigated the protective potential of PHYLN extract loaded into niosomal nanocarriers (PHYLN-NIO) against obesity-induced hepatic steatosis and explored its mechanistic similarity to glucagon-like peptide-1 receptor agonists (GLP-1RAs). Rats were divided into seven groups: control, PHYLN-NIO, HFD, HFD + Semaglutide, HFD + Semaglutide + exendin 9–39, HFD + PHYLN-NIO, and HFD + PHYLN-NIO + exendin 9–39. PHYLN-NIO markedly reduced body weight and body mass index, hepatic steatosis, and inflammation, while enhancing antioxidant status, insulin sensitivity, and lipid profiles. Mechanistically, PHYLN-NIO modulated the lncRNA-MALAT1/miR-206 axis, restored GLP-1/GLP-1R signaling, and downregulated key hepatic lipogenic regulators (LXR-α, SREBP-1c, FASN, ACC-1), while upregulating genes involved in fatty acid oxidation and metabolic homeostasis (FXR, PPAR-α, FOXA2). Notably, co-administration of exendin 9–39 reversed these effects, confirming a GLP-1R-dependent mechanism. These findings suggest that PHYLN-NIO effectively targets MALAT1/miR-206/GLP-1R signaling pathways, demonstrating its potential as a promising nanotherapeutic candidate for MAFLD management.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":"59 1","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13130705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of MICT and HIIT on mitochondrial dynamics-related proteins in visceral adipose tissue of type 2 diabetic rats.","authors":"Mohammad Rahman Rahimi, Ian G Davies, Hadi Golpasandi, Narges Fatahi","doi":"10.1186/s40659-026-00694-x","DOIUrl":"10.1186/s40659-026-00694-x","url":null,"abstract":"<p><p>BACKGROUND: Adipose tissue, as an endocrine gland, significantly influences the pathophysiology of type 2 diabetes (T2DM) through mitochondrial dysfunction. This study examined the effects of two exercise training types on mitochondrial dynamic protein content in visceral adipose tissue (VAT) of T2DM-induced rats. METHODS: Male Wistar rats (total n = 40; 8–10 weeks old, ~ 220 g) were used. Thirty-two rats were fed a high-fat diet (HFD) for 6 weeks and received streptozotocin (STZ) to induce type 2 diabetes mellitus (T2DM). Eight additional rats were maintained on standard chow as the healthy control group (NC, n = 8). The diabetic rats were randomly divided into three groups (n = 8 each): diabetic control (DC), diabetes + MICT (MICT + D), and diabetes + HIIT (HIIT + D). All animals (total n = 40) completed the study and were included in the analyses. MICT involved 8 weeks of training (5 sessions/week, 50 min at 60% maximal speed), while HIIT consisted of 8 weeks (5 sessions/week, 4–7 sets of 4 min at 80–90% maximal speed). Western blot analysis revealed significant increases in mitochondrial fission proteins (Drp-1: 238%, Fis-1: 99%) in the DC group compared to HC (p < 0.05). RESULTS: Both MICT and HIIT significantly reduced Drp-1 (53.55%, 77.81%) and Fis-1 (16.08%, 36.18%) while increasing MFN-2 (26.25%, 57.50%) and OPA-1 (66.10%, 103.39%) compared to DC. HIIT showed greater changes than MICT (p < 0.05). Additionally, fasting serum glucose and HOMA-IR levels were significantly lower in both exercise groups (p < 0.001). CONCLUSIONS: In conclusion, Type 2 diabetes causes changes in the levels of proteins regulating mitochondrial fission and fusion in visceral adipose tissue, which can be improved through MICT and HIIT training, potentially increasing aerobic capacity and glucose metabolism. </p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13255375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of GH18 chitinase in Leishmania braziliensis: expression, structural insights, and implications for vaccine and therapeutic development.","authors":"Maura Rojas-Pirela, Marirene Chacón-Arnaude, Cristóbal Lárez-Velásquez, María Verónica Rojas, Constanza Cardenas, Ana J Cáceres, Luis-Antonio Corchete, Diego Andrade-Alviárez, Luis A Prieto-Rojas, Daniel Salete-Granado, María Á Pérez-Nieto, Wilfredo Quiñones, Paul A M Michels, Miguel Marcos","doi":"10.1186/s40659-026-00685-y","DOIUrl":"10.1186/s40659-026-00685-y","url":null,"abstract":"<p><p>Chitinases, a group of glycosyl hydrolases (GHs), catalyze the degradation of chitin by releasing N-acetylglucosamine subunits. GHs can be found in all three domains of life. Among the three GH families (GH18, GH19, and GH20), GH18 chitinases are the most conserved and extensively studied. These enzymes have been implicated in nutrition, immune modulation, invasion, and virulence across diverse pathogens. In some parasitic protists, GH18 chitinases are essential for transmission. However, in kinetoplastids, including Leishmania spp., these enzymes remain poorly characterized. This study aimed to identify and characterize chitinase across kinetoplastids, with a particular focus on GH18 chitinase in Leishmania braziliensis, the causative agent of muco-cutaneous leishmaniasis. A bioinformatic pipeline was implemented to retrieve and annotate chitinase genes from multiple databases. Catalytic domains and subcellular localization were identified using dedicated computational tools. Phylogenetic relationships were reconstructed in MEGA12 using maximum likelihood and neighbor-joining methods. RNA-seq data were analyzed to evaluate stage-specific expression. Structural models of L. braziliensis GH18 chitinase (Lbr_ChGH18) were created with AlphaFold and subsequently refined. We identified GH18 chitinases genes across Leishmania species and other kinetoplastids, together with GH19 and GH20 chitinase genes. Lbr_ChGH18 was detected across all life-cycle stages, with peak levels in amastigotes. Docking analyses identified closantel, argifin, and argadin as potential inhibitors of Lbr_ChGH18. Epitope prediction revealed conserved B- and T-cell epitopes in GH18 chitinases from Old and New World Leishmania, capable of binding multiple HLA class I and II molecules, highlighting their potential as diagnostic and vaccine candidates. The discovery of GH20 chitinase-like genes in Trypanosoma species offers new insights into the evolution and functional diversification of GHs in kinetoplastids. The high conservation and expression of GH18 chitinases underscore their potential as promising targets for drug and vaccine development against leishmaniasis.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"OGDH mediates α-ketoglutarate-induced follicular development and antioxidative response by interacting with CAT/SOD2.","authors":"Enyuan Huang, Jingyu Zhou, Mengting Hu, Liuhong Zhang, Jiahao Shao, Meng Lv, Fen Miao, Yao Jiang, Nian Li, Jiaqi Li, Xiaolong Yuan","doi":"10.1186/s40659-026-00688-9","DOIUrl":"10.1186/s40659-026-00688-9","url":null,"abstract":"<p><p>BACKGROUND: Follicular disorders, often driven by ROS-induced granulosa cell apoptosis, are a major cause of female infertility. While α-ketoglutarate (AKG), also known as 2-oxoglutarate, can improve follicular development, the underlying mechanisms remain unclear. Given that AKG is the primary substrate of oxoglutarate dehydrogenase (OGDH), this study aimed to investigate how OGDH mediates the protective role of AKG against oxidative stress and in supporting follicular development. RESULT: AKG treatment advanced puberty onset and increased the number of corpora lutea in mice. It alleviated oxidative stress and apoptosis in granulosa cells by upregulating CAT and downregulating P53. Crucially, OGDH physically interacted with CAT and SOD2 and boosted their enzymatic activities, thereby reinforcing AKG’s antioxidative effects. Knockdown of OGDH markedly impaired the ability of AKG to promote follicular development. CONCLUSIONS: These findings identify OGDH as a key mediator of AKG’s protective role in follicular development through modulation of oxidative stress and apoptosis. This work provides mechanistic insight into AKG function and supports its potential as a therapeutic strategy for follicular disorders. </p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13200353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-21 silencing inhibits the proliferation, growth, and migration of colorectal cancer cells via suppressing phosphorylation of ERK1/2 and STAT3.","authors":"Ching Yi Ong, Wen Tao Xiong, Nor Suhada Anuar, Eshtiyag Abdalla Abdalkareem, Ming Thong Ong, Boon Yin Khoo","doi":"10.1186/s40659-026-00692-z","DOIUrl":"10.1186/s40659-026-00692-z","url":null,"abstract":"<p><p>BACKGROUND: This study aimed to elucidate the proliferative and migratory roles of interleukin-21 (IL-21) in HCT-116 and HT-29 colorectal cancer cells using a loss-of-function gene approach. METHODS: The short hairpin ribonucleic acid (shRNA)- and short interfering ribonucleic acid (siRNA)-mediated approaches were used to achieve specific gene silencing in both cell lines. The downstream experiments, including gene silencing efficiency, were then assessed using Western blotting, microscopy, the 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay, the transwell migration assay, cell cycle analysis, the clonogenic assay, and the wound healing assay. RESULTS: Our results revealed that silencing the IL-21 gene significantly suppressed the viability and proliferation of HCT-116 and HT-29 cells. Although IL-21 gene silencing did not induce cell cycle arrest in either cell line, the reduced expression of proliferating cell nuclear antigen (PCNA) upon gene silencing aligned with the proliferation assay results. Additionally, the migration of HCT-116 and HT-29 cells was markedly attenuated upon gene silencing. The restoration of E-cadherin expression in IL-21-silenced cell lines, compared to control cells, indicated decreased receptiveness to epithelial-to-mesenchymal transition (EMT) initiation. Furthermore, IL-21 signalling was found to promote the proliferation and migration of colorectal cancer cells by suppressing the activation and phosphorylation of ERK1/2 and STAT3. CONCLUSION: The pro-tumourigenic properties of IL-21 could serve as a biomarker of tumour aggressiveness in colorectal cancer and provide insights for the development of advanced cancer therapies. </p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13200428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147643961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alternatives for fetal bovine serum (FBS) and sustainability of milk derivatives in cell culture.","authors":"Olga Maria Pittino, Maria Sofia Semprini, Francesca Ruzzi, Stefania Angelicola, Chiara Cappello, Laura Scalambra, Mariateresa Frascino, Patrick L S Michel, Patrizia Nanni, Pier-Luigi Lollini, Arianna Palladini","doi":"10.1186/s40659-026-00691-0","DOIUrl":"10.1186/s40659-026-00691-0","url":null,"abstract":"<p><p>Fetal bovine serum (FBS) is frequently used as a media supplement in cell cultures, as it contains many nutrients, growth factors, and hormones crucial to sustaining cell growth in vitro. However, over the years, concerns about its use have been highlighted. The unknown composition, batch-to-batch variability, and increasing demand and prices have raised scientific and economic issues. In addition, the collection procedure has raised ethical concerns. These issues have prompted researchers worldwide to explore more sustainable and reproducible alternatives performing like FBS. In this review, we examine several potential FBS substitutes, derived from other animal sources or chemically defined sera. Among the considered alternatives, milk emerges as a relevant and suitable option, helping to steer the biotechnological progress towards a more ethical and sustainable approach. Food waste is a globally widespread problem, and milk is no exception. Its use as an alternative supplement for cell cultures could contribute to a reduction in food waste and in the FBS usage, limiting the drawbacks associated with it. Furthermore, milk is often referred to as the “perfect food” as it is rich in nutrients fundamental to sustaining growth, resembling FBS characteristics. Bovine milk derivatives have proven effective in reducing and, in some cases, fully replacing FBS, therefore representing an interesting and feasible option as supplements for culture media. Considering that, requalified milk could help address both social and economic needs and, through circular economy strategies, reduce costs for the biotechnological industry and enhance environmental sustainability.</p>","PeriodicalId":9084,"journal":{"name":"Biological Research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13151094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147572421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}