Advanced biologyPub Date : 2024-10-08DOI: 10.1002/adbi.202400383
Zhuo Pei, Jing Fan, Maolin Tang, Yuhong Li
{"title":"Ferroptosis: A New Strategy for the Treatment of Fibrotic Diseases.","authors":"Zhuo Pei, Jing Fan, Maolin Tang, Yuhong Li","doi":"10.1002/adbi.202400383","DOIUrl":"https://doi.org/10.1002/adbi.202400383","url":null,"abstract":"<p><p>Ferroptosis is a new type of cell death characterized by iron dependence and the excessive accumulation of lipid reactive oxygen species (lipid ROS) that has gradually become better characterized. There is sufficient evidence indicating that ferroptosis is associated with a variety of human life activities and diseases, such as tumor suppression, ischemic organ injury, and degenerative disorders. Notably, ferroptosis is also involved in the initiation and development of fibrosis in various organs, including liver fibrosis, pulmonary fibrosis, renal fibrosis, and cardiac fibrosis, which is usually irreversible and refractory. Although a large number of patients with fibrosis urgently need to be treated, the current treatment options are still limited and unsatisfactory. Organ fibrosis involves a series of complex and orderly processes, such as parenchymal cell damage, recruitment of inflammatory cells and activation of fibroblasts, which ultimately leads to the accumulation of extracellular matrix (ECM) and the formation of fibrosis. An increasing number of studies have confirmed the close association between these pathological processes and ferroptosis. This review summarizes the role and function of ferroptosis in fibrosis and proposes several potential therapeutic strategies and pathways based on ferroptosis.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400383"},"PeriodicalIF":3.2,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387155","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}
Advanced biologyPub Date : 2024-10-08DOI: 10.1002/adbi.202400243
Martin Grunwald, Welda P M Pasatu, Jente Spille, Rene Haensel, Jens Stieler, Max Holzer, Mirjana Ziemer, Kevin H G Butz, Sven Martin, Stephanie Margarete Mueller, Markus Morawski
{"title":"Number of Facial Hair Corresponds to Frequency of Spontaneous Face-Touch in Humans.","authors":"Martin Grunwald, Welda P M Pasatu, Jente Spille, Rene Haensel, Jens Stieler, Max Holzer, Mirjana Ziemer, Kevin H G Butz, Sven Martin, Stephanie Margarete Mueller, Markus Morawski","doi":"10.1002/adbi.202400243","DOIUrl":"https://doi.org/10.1002/adbi.202400243","url":null,"abstract":"<p><p>People all over the world, independent of their culture or background, touch their faces up to 800 times per day. No other part of the body is touched as often as the face. Forehead, nose, and chin-the so-called T-zone of the face-are touched particularly frequently during spontaneous facial self-touches (sFST). It is hypothesized that there is a relationship between the density of mechanoreceptors (inferred from facial hair distribution) and the frequency of spontaneous self-touching. In order to indirectly measure the density of mechanoreceptors (cutaneous end organ complexes), the number of vellus and terminal hairs at 40 different measuring points on the face of 30 (15f/15m) healthy volunteers in study A is determined. In study B, the frequency of sFST at the same 40 measuring points in 66 (32f/34m) healthy persons is determined. Study A reveals that the number of facial hairs-in both sexes-is higher in the T-zone than in other areas of the face. Study B reveals that the T-zone is touched more frequently than other areas of the face. Skin areas of the face with a higher number of vellus hairs (and presumably higher innervation density) are touched particularly frequently during sFST.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400243"},"PeriodicalIF":3.2,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387156","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}
Advanced biologyPub Date : 2024-10-04DOI: 10.1002/adbi.202400090
Shujia Song, Fuxing Li, Bingxiang Zhao, Min Zhou, Xiaobo Wang
{"title":"Ultraviolet Light Causes Skin Cell Senescence: From Mechanism to Prevention Principle.","authors":"Shujia Song, Fuxing Li, Bingxiang Zhao, Min Zhou, Xiaobo Wang","doi":"10.1002/adbi.202400090","DOIUrl":"https://doi.org/10.1002/adbi.202400090","url":null,"abstract":"<p><p>The skin is an effective protective barrier that significantly protects the body from damage caused by external environmental factors. Furthermore, skin condition significantly affects external beauty. In today's era, which is of material and spiritual prosperity, there is growing attention on skincare and wellness. Ultraviolet radiation is one of the most common external factors that lead to conditions like sunburn, skin cancer, and skin aging. In this review, several mechanisms of UV-induced skin cell senescence are discussed, including DNA damage, oxidative stress, inflammatory response, and mitochondrial dysfunction, which have their own characteristics and mutual effects. As an illustration, mitochondrial dysfunction triggers electron evasion and the generation of more reactive oxygen species, leading to oxidative stress and the activation of the NLRP3 inflammasome, which in turn causes mitochondrial DNA (mt DNA) damage. Based on the current mechanism, suitable prevention and treatment strategies are proposed from sunscreen, dietary, and experimental medications respectively, aimed at slowing down skin cell aging and providing protection from ultraviolet radiation. The effects of ultraviolet rays on skin is summarized, offering insights and directions for future studies on mechanism of skin cell senescence, with an anticipation of discovering more effective prevention and cure methods.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400090"},"PeriodicalIF":3.2,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370728","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}
Advanced biologyPub Date : 2024-09-27DOI: 10.1002/adbi.202400180
Hua Liu, Qiyu Yue, Wenyue Zhang, Qi Ding, Junjie Yang, Mu Lin, Jia Sun
{"title":"Xinglou Chengqi Decoction Protects against Cerebral Ischemia/Reperfusion Injury by Inhibiting Ferroptosis via SLC7A11/GPX4 Signaling","authors":"Hua Liu, Qiyu Yue, Wenyue Zhang, Qi Ding, Junjie Yang, Mu Lin, Jia Sun","doi":"10.1002/adbi.202400180","DOIUrl":"10.1002/adbi.202400180","url":null,"abstract":"<p>Xinglou Chengqi decoction (XLCQD) is a Chinese formula that offers benefits in ischemic stroke. However, the underlying mechanism of the effects of XLCQD-mediated anti-ischemic stroke effects remains obscure. This study investigates the ferroptosis mechanism of XLCQD against cerebral ischemia/reperfusion (I/R) injury using rat models of middle cerebral artery occlusion/reperfusion (MCAO/R). Ferroptosis differs from traditional cell death pathways and is linked to oxidative stress-induced lipid peroxidation and glutathione (GSH) depletion, which is essential to the development of ischemic stroke. In this study, it is shown that XLCQD improves brain infarction, neurological dysfunction, and histopathological changes caused by MCAO/R exposure, and improving I/R-induced oxidative damage through inhibition of ferroptosis via (Solute Carrier Family 7 Member 11) SLC7A11/ (glutathione peroxidase 4) GPX4 pathway. Interestingly, it is found that XLCQD-mediated protection in I/R is reversed by the silence of SLC7A11. XLCQD intervention significantly promotes GSH content and suppresses Reactive Oxygen Species(ROS), iron accumulation, as well as Malondialdehyde (MDA) generation, are markedly abrogated when SLC7A11 is knockdown by SLC7A11-shRNA transfection, indicating that SLC7A11 is the main target of XLCQD to further trigger intracellular events. In conclusion, XLCQD attenuates in vivo cerebral I/R injury by reducing ferroptosis via the SLC7A11/GPX4 pathway.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"8 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339137","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}
Advanced biologyPub Date : 2024-09-27DOI: 10.1002/adbi.202400353
Arjan Hazegh Nikroo, Wiggert J Altenburg, Thijs W van Veldhuisen, Luc Brunsveld, Jan C M van Hest
{"title":"Spatiotemporal Control Over Protein Release from Artificial Cells via a Light-Activatable Protease.","authors":"Arjan Hazegh Nikroo, Wiggert J Altenburg, Thijs W van Veldhuisen, Luc Brunsveld, Jan C M van Hest","doi":"10.1002/adbi.202400353","DOIUrl":"https://doi.org/10.1002/adbi.202400353","url":null,"abstract":"<p><p>The regulation of protein uptake and secretion by cells is paramount for intercellular signaling and complex multicellular behavior. Mimicking protein-mediated communication in artificial cells holds great promise to elucidate the underlying working principles, but remains challenging without the stimulus-responsive regulatory machinery of living cells. Therefore, systems to precisely control when and where protein release occurs should be incorporated in artificial cells. Here, a light-activatable TEV protease (LaTEV) is presented that enables spatiotemporal control over protein release from a coacervate-based artificial cell platform. Due to the presence of Ni<sup>2+</sup>-nitrilotriacetic acid moieties within the coacervates, His-tagged proteins are effectively sequestered into the coacervates. LaTEV is first photocaged, effectively blocking its activity. Upon activation by irradiation with 365 nm light, LaTEV cleaves the His-tags from sequestered cargo proteins, resulting in their release. The successful blocking and activation of LaTEV provides control over protein release rate and triggerable protein release from specific coacervates via selective irradiation. Furthermore, light-activated directional transfer of proteins between two artificial cell populations is demonstrated. Overall, this system opens up avenues to engineer light-responsive protein-mediated communication in artificial cell context, which can advance the probing of intercellular signaling and the development of protein delivery platforms.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400353"},"PeriodicalIF":3.2,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339136","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}
Advanced biologyPub Date : 2024-09-23DOI: 10.1002/adbi.202470093
{"title":"RETRACTION: Bioreactors Based on Enzymes Encapsulated in Photoresponsive Transformable Nanotubes and Nanocoils End-Capped with Magnetic Nanoparticles","authors":"","doi":"10.1002/adbi.202470093","DOIUrl":"https://doi.org/10.1002/adbi.202470093","url":null,"abstract":"<p><b>RETRACTION</b>: N. Kameta, Y. Manaka, H. Akiyama, T. Shimizu, “Bioreactors Based on Enzymes Encapsulated in Photoresponsive Transformable Nanotubes and Nanocoils End-Capped with Magnetic Nanoparticles,” Advanced Biosystems 2, no. 4 (2018): 1700214, https://doi.org/10.1002/adbi.201700214.</p><p>The above article, published online on 1 February 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, Naohiro Kameta, Yuichi Manaka, Haruhisa Akiyama and Toshimi Shimizu; the journal Editor-in-Chief, Monty Montano; and Wiley-VCH GmbH, Weinheim. The retraction has been agreed upon following an investigation into concerns raised by National Institute of Advanced Industrial Science and Technology (AIST), and also requested by all authors due to image falsification and fabrication in electron microscopy images. In Figure 2a and 2f, where the first author falsified TEM images of irrelevant nanotubes that were developed by the authors in other studies; in Figures 2b and 2c, where the first author carelessly placed incorrect scale bars and scale values; all affecting the interpretation of the data and research results presented.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"8 10","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/adbi.202470093","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142439018","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}
Advanced biologyPub Date : 2024-09-15DOI: 10.1002/adbi.202470091
Esra Türker, Mateo S. Andrade Mier, Jessica Faber, Selma J. Padilla Padilla, Nicoletta Murenu, Philipp Stahlhut, Gregor Lang, Zan Lamberger, Jeanette Weigelt, Natascha Schaefer, Jörg Tessmar, Pamela L. Strissel, Torsten Blunk, Silvia Budday, Reiner Strick, Carmen Villmann
{"title":"Breast Tumor Cell Survival and Morphology in a Brain-like Extracellular Matrix Depends on Matrix Composition and Mechanical Properties (Adv. Biology 9/2024)","authors":"Esra Türker, Mateo S. Andrade Mier, Jessica Faber, Selma J. Padilla Padilla, Nicoletta Murenu, Philipp Stahlhut, Gregor Lang, Zan Lamberger, Jeanette Weigelt, Natascha Schaefer, Jörg Tessmar, Pamela L. Strissel, Torsten Blunk, Silvia Budday, Reiner Strick, Carmen Villmann","doi":"10.1002/adbi.202470091","DOIUrl":"https://doi.org/10.1002/adbi.202470091","url":null,"abstract":"<p><b>Breast Tumor Cells</b></p><p>Triple-negative breast cancer (TNBC) is the most invasive type of breast cancer with a high risk of brain metastasis. In article number 2400184, Carmen Villmann and co-workers systematically set up a 3D cellular system to study TNBC in a biomimetic brain surrounding in terms of cell–cell and cell–matrix interactions. 3D disease model for breast tumor cells (green) attached to collagen (red, confocal image) grown in thiolated hyaluronic acid-based hydrogel (background image black). Icons represent MEW PCL scaffolds, PEGAcr crosslinker, different extracellular matrix (ECM) proteins (collagen, fibronectin, laminin). ECM supplementation is the key regulator of cellular morphology behaviour and survival. The original confocal image was modified using an art filter.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"8 9","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/adbi.202470091","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142234721","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":"SIK2: A Novel Negative Feedback Regulator of FGF2 Signaling","authors":"Gamze Kuser-Abali, Asli Ugurlu-Bayarslan, Yeliz Yilmaz, Ferruh Ozcan, Funda Karaer, Kuyas Bugra","doi":"10.1002/adbi.202400032","DOIUrl":"10.1002/adbi.202400032","url":null,"abstract":"<p>A wide range of cells respond to fibroblast growth factor 2 (FGF2) by proliferation via activation of the Ras/ERK1/2 pathway. In this study, the potential involvement of salt inducible kinase SIK2) in this cascade within retinal Müller glia is explored. It is found that SIK2 phosphorylation status and activity are modulated in an FGF2-dependent manner, possibly via ERK1/2. With SIK2 downregulation, enhanced ERK1/2 activation with delayed attenuation and increased cell proliferation is observed, while SIK2 overexpression hampers FGF2-dependent ERK1/2 activation. In vitro kinase and site-directed mutagenesis studies indicate that SIK2 targets the pathway element GRB2-associated-binding protein 1 (Gab1) on Ser266. This phosphorylation event weakens Gab1 interactions with its partners growth factor receptor-bound protein 2 (Grb2) and Src homology region 2 domain containing phosphatase 2 (Shp2). Collectively, these results suggest that during FGF2-dependent proliferation process ERK1/2-mediated activation of SIK2 targets Gab1, resulting in downregulation of the Ras/ERK1/2 cascade in a feedback loop.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"8 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278754","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}
Advanced biologyPub Date : 2024-09-12DOI: 10.1002/adbi.202400278
Diksha Jawale, Shweta Khandibharad, Shailza Singh
{"title":"Innate Immune Response and Epigenetic Regulation: A Closely Intertwined Tale in Inflammation.","authors":"Diksha Jawale, Shweta Khandibharad, Shailza Singh","doi":"10.1002/adbi.202400278","DOIUrl":"https://doi.org/10.1002/adbi.202400278","url":null,"abstract":"<p><p>Maintenance of delicate homeostasis is very important in various diseases because it ensures appropriate immune surveillance against pathogens and prevents excessive inflammation. In a disturbed homeostatic condition, hyperactivation of immune cells takes place and interplay between these cells triggers a plethora of signaling pathways, releasing various pro-inflammatory cytokines such as Tumor necrosis factor alpha (TNFα), Interferon-gamma (IFNƴ), Interleukin-6 (IL-6), and Interleukin-1 beta (IL-1β), which marks cytokine storm formation. To be precise, dysregulated balance can impede or increase susceptibility to various pathogens. Pathogens have the ability to hijack the host immune system by interfering with the host's chromatin architecture for their survival and replication in the host cell. Cytokines, particularly IL-6, Interleukin-17 (IL-17), and Interleukin-23 (IL-23), play a key role in orchestrating innate immune responses and shaping adaptive immunity. Understanding the interplay between immune response and the role of epigenetic modification to maintain immune homeostasis and the structural aspects of IL-6, IL-17, and IL-23 can be illuminating for a novel therapeutic regimen to treat various infectious diseases. In this review, the light is shed on how the orchestration of epigenetic regulation facilitates immune homeostasis.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400278"},"PeriodicalIF":3.2,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278752","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}