Article
Biochemistry & Molecular Biology
Ting-An Yie, Cynthia A. Loomis, Johannes Nowatzky, Alireza Khodadadi-Jamayran, Ziyan Lin, Michael Cammer, Clea Barnett, Valeria Mezzano, Mark Alu, Jackson A. Novick, John S. Munger, Matthias C. Kugler
Summary: Normal lung development relies on the coordinated action of HH and PDGF signaling pathways, which are crucial for mesenchymal differentiation and proliferation. Recent studies have shown that HH is necessary for alveolar myofibroblast differentiation. In this study, we investigated the relationship between HH and PDGF signaling during postnatal lung development in mice. Our findings suggest that HH and PDGF signaling pathways intersect to support myofibroblast function during secondary alveolar septum formation.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2023)
Review
Cardiac & Cardiovascular Systems
Nikolaos G. Frangogiannis
Summary: Myocardial fibrosis, characterized by the expansion of cardiac interstitium through deposition of extracellular matrix proteins, is a common pathophysiologic feature in various myocardial conditions. Activated fibroblasts and myofibroblasts play a central role in cardiac fibrosis, producing matrix proteins and triggering fibrogenic signalling cascades in response to stress. Immune cells, vascular cells, and cardiomyocytes can also contribute to fibrosis, while fibrotic changes may disrupt cardiac function and play a role in arrhythmogenesis.
CARDIOVASCULAR RESEARCH
(2021)
Review
Pharmacology & Pharmacy
Xiaoying Yin, Xinxin Yin, Xin Pan, Jingyu Zhang, Xinhui Fan, Jiaxin Li, Xiaoxuan Zhai, Lijun Jiang, Panpan Hao, Jiali Wang, Yuguo Chen
Summary: Cardiac fibrosis is essential for cardiac tissue homeostasis and repair after myocardial infarction. The differentiation of cardiac fibroblasts into myofibroblasts and the deposition of extracellular matrix collagen are the hallmarks of cardiac fibrosis, which are regulated by multiple signaling pathways and different types of cells. Understanding the development of cardiac fibrosis after myocardial infarction has advanced in both basic and clinical research, and the regulation of fibrotic remodeling may lead to new diagnostic and therapeutic strategies for improved outcomes. This article aims to elaborate on the pathophysiology, examination, and intervention of cardiac fibrosis after myocardial infarction.
FRONTIERS IN PHARMACOLOGY
(2023)
Review
Cell Biology
Ravi K. Adapala, Venkatesh Katari, Lakshminarayan Reddy Teegala, Sathwika Thodeti, Sailaja Paruchuri, Charles K. Thodeti
Summary: The review discusses the mechanism of fibrosis and proposes TRPV4 as a potential therapeutic target for the condition, highlighting the need for specific drugs in the treatment of fibrosis.
Review
Cell Biology
Harikrishnan Venugopal, Anis Hanna, Claudio Humeres, Nikolaos G. Frangogiannis
Summary: This review discusses the mechanisms, roles, and fate of fibroblasts in the infarcted heart. Following a myocardial infarction, fibroblasts undergo phenotypic transitions and contribute to inflammatory, reparative, and angiogenic responses. They form collagen-based scars to protect the infarcted ventricle and may also stimulate angiogenesis. Prolonged activation of fibroblasts may contribute to adverse remodeling and heart failure.
Article
Pharmacology & Pharmacy
Jian Sun, Tongzhu Jin, Zhihui Niu, Jiayu Guo, Yingying Guo, Ruoxuan Yang, Qianqian Wang, Huiying Gao, Yuhan Zhang, Tianyu Li, Wenxin He, Zhixin Li, Wenchao Ma, Wei Su, Liangliang Li, Xingxing Fan, Hongli Shan, Haihai Liang
Summary: This study found that lncRNA DACH1 is downregulated in patients with pulmonary fibrosis and in a mouse model of the disease. LncDACH1 inhibits lung fibrosis by interacting with SRSF1 to suppress CTNNB1 accumulation.
ACTA PHARMACEUTICA SINICA B
(2022)
Review
Biochemistry & Molecular Biology
Min Gao, Jing Wang, Jianghua Zang, Yina An, Yanjun Dong
Summary: Renal fibrosis is a hallmark of CKD, with unresolved renal inflammation playing a key role in promoting fibrotic processes. Various T cells and macrophages are central players in the inflammatory microenvironment and fibrotic process.
Review
Biochemistry & Molecular Biology
Kealan McElhinney, Mustapha Irnaten, Colm O'Brien
Summary: Fibrosis is a dysregulated wound repair response that leads to progressive disruption of tissue architecture and significant morbidity/mortality. Current treatments can slow disease progression but not restore organ function or reverse fibrotic changes. Myofibroblast apoptosis is absent in fibrosis, contributing to persistent myofibroblast activation and perpetuation of the disease.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Pharmacology & Pharmacy
Menglin Zou, Jingfeng Zou, Xingxing Hu, Weishuai Zheng, Mingyang Zhang, Zhenshun Cheng
Summary: The elevated expression of LTBP2 plays a critical role in pulmonary fibrosis (PF) and contributes to fibroblast-to-myofibroblast differentiation. Silencing LTBP2 protects against PF and suppresses the differentiation of fibroblasts into myofibroblasts. Meanwhile, overexpression of LTBP2 induces this differentiation process even in the absence of TGF beta 1, indicating a potential therapeutic target for PF.
FRONTIERS IN PHARMACOLOGY
(2021)
Review
Biochemistry & Molecular Biology
Izabela Tuleta, Nikolaos G. Frangogiannis
Summary: Diabetes-related morbidity and mortality are mainly caused by complications of the disease such as heart and renal failure, hepatic insufficiency, retinopathy, and neuropathy. Fibrosis, excessive deposition of extracellular matrix in tissues, is common in advanced diabetes and may lead to organ dysfunction. Various factors like hyperglycemia, lipotoxic injury, and insulin resistance trigger fibrotic responses through multiple pathways, affecting different organs differently. Targeting these pathways for anti-fibrotic therapies in diabetic patients poses both promises and challenges.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2021)
Article
Biochemistry & Molecular Biology
Valentina S. Glazieva, Natalya A. Alexandrushkina, Peter P. Nimiritsky, Maria A. Kulebyakina, Roman Yu. Eremichev, Pavel I. Makarevich
Summary: This study aimed to investigate factors affecting the assembly time of cell sheet (CS). Through testing adipose-derived mesenchymal stromal cells (MSCs) from 14 healthy individuals, it was found that high contents of collagen I and collagen IV were associated with prolonged assembly time. Furthermore, MSCs with shorter lag phase assembled faster, while factors such as age, sex, fibronectin showed no significant correlation with assembly time.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Biochemistry & Molecular Biology
Lejla Medzikovic, Hylja Heese, Pieter B. van Loenen, Cindy P. A. A. van Roomen, Ingeborg B. Hooijkaas, Vincent M. Christoffels, Esther E. Creemers, Carlie J. M. de Vries, Vivian de Waard
Summary: Nur77 regulates cardiac fibrosis by promoting CF-to-MyoFB transition intrinsically and inhibiting cardiomyocyte-driven paracrine TGF-beta-mediated MyoFB differentiation.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Engineering, Biomedical
Harsha Kabra, Tanaya Walimbe, Kate Stuart, Camille Indey, Swati Jalgaonkar, Elvis Ikwa, Taylor Skurnac, Julia Chen, Andrew Woolley, Nicholas M. Snead, Nathan Bachtell, Diana J. Leeming, Morten Karsdal, Glenn Prestwich, Alyssa Panitch, John Paderi
Summary: SBR-294, targeting collagen-mediated platelet activation and PDGF activity, showed potential therapeutic benefits in reducing liver fibrosis in the CCl4 mouse model. Further investigation is warranted to explore its potential as a treatment for liver fibrosis.
Review
Pathology
Richard S. Nho, Megan N. Ballinger, Mauricio M. Rojas, Samir N. Ghadiali, Jeffrey C. Horowitz
Summary: Lung fibrosis is characterized by the accumulation of ECM proteins by apoptosis-resistant fibroblasts. Lung epithelial injury leads to fibroblast recruitment and activation, which are necessary for tissue repair. However, under pathological conditions, a vicious cycle of profibrotic factors and cell-matrix signaling promotes the development of lung fibrosis characterized by increased ECM proteins and changes in matrix properties. Understanding the role of ECM in fibrosis can lead to new therapeutic targets and improved outcomes.
AMERICAN JOURNAL OF PATHOLOGY
(2022)
Article
Medicine, Research & Experimental
Xiaoyan Wu, Xiulian Miao, Tinghui Shao, Shifan Tang, Yanshan Lin, Yong Xu, Nan Li, Tao Zhang
Summary: This study reveals that Slug is involved in regulating fibroblast-myofibroblast transition and renal fibrosis by modulating the expression of key transcription factors and ROS levels.
Letter
Gastroenterology & Hepatology
Ralf Weiskirchen
Article
Pathology
Katja Ermert, Eva M. Buhl, Barbara M. Klinkhammer, Juergen Floege, Peter Boor
Summary: In chronic kidney disease (CKD), the endothelial glycocalyx (EG) experiences structural and functional changes. The study investigated the ultrastructural alterations of the EG in different CKD models and found reduced binding and significant pathologic alterations in peritubular capillaries.
AMERICAN JOURNAL OF PATHOLOGY
(2023)
Article
Urology & Nephrology
Ting Jia, Tong Xu, Bart Smeets, Eva Miriam Buhl, Marcus Johannes Moeller, Juergen Floege, Barbara Mara Klinkhammer, Peter Boor
Summary: The study suggests that PDGF-B and its receptor PDGFR-beta play a crucial role in the development and progression of FSGS by affecting the activation, proliferation, and fibrotic characteristics of PECs. The molecular crosstalk between podocytes and PECs mediated by PDGF-B and PDGFR-beta drives glomerulosclerosis and the progression of FSGS. Treatment with PDGF-B neutralizing antibody can improve kidney function and reduce the occurrence of FSGS.
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
(2023)
Article
Multidisciplinary Sciences
David L. Hoelscher, Nassim Bouteldja, Mehdi Joodaki, Maria L. Russo, Yu-Chia Lan, Alireza Vafaei Sadr, Mingbo Cheng, Vladimir Tesar, Saskia V. Stillfried, Barbara M. Klinkhammer, Jonathan Barratt, Juergen Floege, Ian S. D. Roberts, Rosanna Coppo, Ivan G. Costa, Roman D. Buelow, Peter Boor
Summary: Pathology diagnostics still rely on tissue morphology assessment by trained experts. Here, the authors perform deep-learning-based segmentation followed by large-scale feature extraction of histological images, i.e., next-generation morphometry, to enable outcome-relevant and disease-specific pathomics analysis of non-tumor kidney pathology.
NATURE COMMUNICATIONS
(2023)
Article
Biochemistry & Molecular Biology
Louis C. Penning, Marina Berenguer, Anna Czlonkowska, Kay L. Double, Petr Dusek, Carmen Espinos, Svetlana Lutsenko, Valentina Medici, Wiebke Papenthin, Wolfgang Stremmel, Jose Willemse, Ralf Weiskirchen
Summary: Wilson disease is a rare inherited metabolic disorder with diverse clinical presentations affecting the liver, neurological system, psychiatric status, and vision, often in combination. Mutations in the ATP7B gene lead to copper accumulation in hepatocytes and/or neurons, making clinical diagnosis challenging. Diagnosis is complicated by mild and non-specific manifestations, mutations with unclear effects on protein function, and ambiguous laboratory tests, particularly concerning serum ceruloplasmin levels. Establishing a global collaboration of researchers, clinicians, and patient advocacy groups is crucial for identifying and addressing the outstanding challenges of Wilson disease.
Review
Nutrition & Dietetics
Bodo C. C. Melnik, Swen Malte John, Pedro Carrera-Bastos, Loren Cordain, Claus Leitzmann, Ralf Weiskirchen, Gerd Schmitz
Summary: This review evaluates the impact of cow milk on breast carcinogenesis by linking recent epidemiological evidence and new insights into the molecular signaling of milk and its constituents in breast cancer pathogenesis. Recent prospective cohort studies support the association between cow's milk consumption and the risk of estrogen receptor-alpha-positive breast cancer. Milk contains various components that can increase systemic insulin-like growth factor 1, insulin, and estrogen signaling, promoting breast cancer. Potential oncogenic components of commercial milk include exosomal microRNAs, bovine meat and milk factors, aflatoxin M1, bisphenol A, pesticides, and micro- and nanoplastics. Individuals with certain gene mutations and genetic polymorphisms may be at increased risk for milk-induced breast cancer.
CURRENT NUTRITION REPORTS
(2023)
Article
Cell Biology
Lilach Barer, Sarah K. Schroeder, Ralf Weiskirchen, Eran Bacharach, Marcelo Ehrlich
Summary: Lipocalin-2 (LCN2) has pleiotropic functions in different types of cancers. This study found that LCN2 can regulate prostate cancer cells by affecting cytoskeleton organization and expression of inflammation mediators. It also showed that LCN2 can modulate prostate cancer cell susceptibility to oncolytic viruses by attenuating PERK activity and increasing interferon and interferon-stimulated gene expression.
EUROPEAN JOURNAL OF CELL BIOLOGY
(2023)
Article
Immunology
Mihael Vucur, Ahmed Ghallab, Anne T. Schneider, Arlind Adili, Mingbo Cheng, Mirco Castoldi, Michael T. Singer, Veronika Buettner, Leonie S. Keysberg, Lena Kuesgens, Marlene Kohlhepp, Boris Goerg, Suchira Gallage, Jose Efren Barragan Avila, Kristian Unger, Claus Kordes, Anne-Laure Leblond, Wiebke Albrecht, Sven H. Loosen, Carolin Lohr, Markus S. Joerdens, Anne Babler, Sikander Hayat, David Schumacher, Maria T. Koenen, Olivier Govaere, Mark Boekschoten, Simone Joers, Carlos Villacorta-Martin, Vincenzo Mazzaferro, Josep M. Llovet, Ralf Weiskirchen, Jakob N. Kather, Patrick Starlinger, Michael Trauner, Mark Luedde, Lara R. Heij, Ulf P. Neumann, Verena Keitel, Johannes G. Bode, Rebekka K. Shneider, Frank Tacke, Bodo Levkau, Twan Lammers, Georg Fluegen, Theodore Alexandrov, Amy L. Collins, Glyn Nelson, Fiona Oakley, Derek A. Mann, Christoph Roderburg, Thomas Longerich, Achim Weber, Augusto Villanueva, Andre L. Samson, James M. Murphy, Rafael Kramann, Fabian Geisler, Ivan G. Costa, Jan G. Hengstle, Mathias Heikenwalder, Tom Luedde
Summary: A molecular switch in hepatocytes can reprogram between two forms of necroptosis signaling, which fundamentally impacts immune responses and hepatocarcinogenesis.
Review
Cell Biology
Sabine Weiskirchen, Sarah K. K. Schroeder, Eva Miriam Buhl, Ralf Weiskirchen
Summary: The cultivation of cells in a favorable artificial environment has become an essential tool in cellular and molecular biology research. However, cell lines are often affected by misidentification, contamination, and specific biological and chemical hazards. This review offers an introduction to common problems encountered in cell culture laboratories and provides guidelines for preventing and addressing these issues.
Article
Information Science & Library Science
Mahsa Keshavarz-Fathi, Niloufar Yazdanpanah, Sajad Kolahchi, Heliya Ziaei, Gary L. Darmstadt, Tommaso Dorigo, Filip Dochy, Lisa Levin, Visith Thongboonkerd, Shuji Ogino, Wei-Hsin Chen, Matjaz Perc, Mark S. Tremblay, Bolajoko O. Olusanya, Idupulapati M. Rao, Nikos Hatziargyriou, Maziar Moradi-Lakeh, Federico Bella, Laszlo Rosivall, Amir H. Gandomi, Armin Sorooshian, Manoj Gupta, Ciprian Gal, Andres M. Lozano, Connie Weaver, Michael Tanzer, Alessandro Poggi, Sadaf G. Sepanlou, Ralf Weiskirchen, Anet Rezek Jambrak, Pedro J. Torres, Esra Capanoglu, Francisco J. Barba, Chua Kian Jon Ernest, Mariano Sigman, Stefano Pluchino, Gevork B. Gharehpetian, Seyed-Mohammad Fereshtehnejad, Muh-Hwa Yang, Sabu Thomas, Wenju Cai, Elisabetta Comini, Neil J. Scolding, Paul S. Myles, Juan J. Nieto, George Perry, Constantine Sedikides, Nima Rezaeia
Summary: Scientometrics and bibliometrics are subfields of library and information science that study the quantity and quality of research outputs. The h-index is the most well-known scientometric index, but it relies on the count of highly cited publications. To address this limitation, we developed a new index called the Universal Research Index (UR-Index) that considers the impact of every single publication. We incorporated additional variables such as publication type, leading role, co-author count, and source metrics into the UR-Index. However, we recognize that unconscious biases in these variables may disadvantage research from specific groups, and encourage efforts to improve equitable scholarly impact in science and academia.
JOURNAL OF ACADEMIC LIBRARIANSHIP
(2023)
Article
Biochemistry & Molecular Biology
Jan C. Kessel, Ralf Weiskirchen, Sarah K. Schroeder
Summary: Estrogen receptor alpha (ERa) is expressed in reproductive and non-reproductive tissues, and its impact on lipocalin 2 (LCN2) expression varies among tissues. This study found an inverse correlation between ERa and LCN2 expression in reproductive tissues, particularly in Esr1-deficient ovaries. However, no significant differences in LCN2 expression were observed in non-reproductive tissues. These findings provide insight into LCN2 regulation in relation to hormones and health.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
Barbara Mara Klinkhammer, Peter Boor
Summary: An increasing number of patients worldwide suffers from chronic kidney disease (CKD). Currently, there is no specific antifibrotic therapy for kidney patients and invasive renal biopsy remains the only option for specific detection and quantification of kidney fibrosis. This review discusses emerging diagnostic approaches and potential therapeutic options for fibrosis, as well as the importance of translational research in establishing fibrosis-specific endpoints for clinical trials.
MOLECULAR ASPECTS OF MEDICINE
(2023)
Article
Biochemistry & Molecular Biology
Ralf Weiskirchen, Sarah K. Schroeder, Sabine Weiskirchen, Eva Miriam Buhl, Bodo Melnik
Summary: Extracellular vesicles, such as exosomes, are small bilayered biovesicles released by cells, enriched with biologically active components. Milk exosomes play a key role in infant growth and development, while exosomes derived from different cell types have regenerative and immunomodulatory properties. Isolation protocols for milk exosomes allow the purification of highly enriched fractions, expressing typical exosomal protein markers.
Article
Mathematical & Computational Biology
Roman D. Buelow, David L. Hoelscher, Ivan G. Costa, Peter Boor
NPJ SYSTEMS BIOLOGY AND APPLICATIONS
(2023)
Article
Gastroenterology & Hepatology
Mohamed Ramadan Mohamed, Johannes Haybaeck, Hanghang Wu, Huan Su, Matthias Bartneck, Cheng Lin, Mark V. Boekschoten, Peter Boor, Benjamin Goeppert, Christian Rupp, Pavel Strnad, Roger J. Davis, Francisco Javier, Christian Trautwein
Summary: This study investigated the role of JNK1/2 during cholestasis and its hepatocyte-specific function. The results showed that Jnk1 and Jnk2 work together to protect hepatocytes from cholestatic liver disease by controlling Apelin signalling. Blocking Apelin signalling attenuated liver injury and fibrosis induced by cholestasis. Targeting Jnk1/2 in hepatocytes may be a new molecular strategy for treating cholestatic liver disease.
