Article
Biochemistry & Molecular Biology
Yuan Liu, Michael J. Jurczak, Travis B. Lear, Bo Lin, Mads B. Larsen, Jason R. Kennerdell, Yanwen Chen, Brydie R. Huckestein, Matthew K. Nguyen, Ferhan Tuncer, Yu Jiang, Satdarshan P. Monga, Christopher P. O'Donnell, Toren Finkel, Bill B. Chen, Rama K. Mallampalli
Summary: A newly discovered compound, BC1618, inhibits the degradation of phosphorylated Ampk alpha by targeting the protein Fbxo48, thereby enhancing Ampk biological activity and promoting mitochondrial fission, autophagy, and improved insulin sensitivity in obese mice. This study reveals a novel pathway for regulating Ampk activity.
NATURE CHEMICAL BIOLOGY
(2021)
Review
Cell Biology
Dora Visnjic, Hrvoje Lalic, Vilma Dembitz, Barbara Tomic, Tomislav Smoljo
Summary: AICAr is commonly used as a pharmacological modulator of AMPK activity, but some effects attributed to AMPK activation have been found to be AMPK-independent. Caution is needed when interpreting studies based on AICAr, especially in the context of understanding the AMPK signaling pathway.
Article
Oncology
Siyuan Yan, Dongdong Yuan, Qianqian Li, Shi Li, Fan Zhang
Summary: Numerous studies have shown the importance of PFKFB3 in glycolysis regulation. PFK-15 inhibitor induces cell death and affects autophagy and protein degradation pathways. AICAR can restore AMPK activity and autophagy while enhancing cell death caused by PFK-15. Additionally, AICAR attenuates the inhibitory effect of PFK-15 on the AKT-mTORC1 signaling pathway.
Article
Anatomy & Morphology
U. Ajay Krishnan, Periyasamy Viswanathan, Anuradha Carani Venkataraman
Summary: The activation of AMPK by AICAR has been found to alleviate symptoms of NAFLD. In a mouse model, AICAR reduced lipid levels in the liver, improved oxidative stress, and upregulated FOXO3 and p-AMPK expression while downregulating p-mTOR expression. These findings reveal the crosstalk between AMPK, mTOR, and FOXO3, providing new insights into the treatment of NAFLD.
Article
Pharmacology & Pharmacy
Yihai Liu, Mingyue Wu, Jiamin Xu, Biao Xu, Lina Kang
Summary: The study demonstrated that the SGLT2 inhibitor empagliflozin could improve cardiac remodeling in early myocardial infarction of non-diabetic mice by reducing cardiomyocyte apoptosis, oxidative stress, and restoring mitochondrial membrane potential. The activation of AMP-activated protein kinase (AMPK) signaling pathway may mediate the cardioprotective role of empagliflozin.
EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES
(2021)
Article
Cell Biology
Arindam Mondal, Jacques Roberge, John Gilleran, Youyi Peng, Dongxuan Jia, Moumen Akel, Yash Patel, Harrison Zoltowski, Anupama Doraiswamy, John Langenfeld
Summary: This study reveals that inhibition of BMP signaling combined with mitochondrial targeting agents induces AIF caspase-independent cell death, primarily through the hyperactivation of AMPK. This is an infrequently studied cell death pathway in cancer.
CELL COMMUNICATION AND SIGNALING
(2022)
Article
Biotechnology & Applied Microbiology
Wenying Chen, Fengting Huang, Jing Huang, Yuanhua Li, Juanfei Peng, Yanyan Zhuang, Xianxian Huang, Liting Lu, Zhe Zhu, Shineng Zhang
Summary: This study revealed that SLC45A4 inhibits autophagy via the AMPK/ULK1 axis in TP53 mutant PDA, suggesting it may serve as a promising biomarker and therapeutic target in TP53 mutant PDA.
JOURNAL OF GENE MEDICINE
(2021)
Article
Cell Biology
Jingang Hou, Yeejin Yun, Changhao Cui, Sunchang Kim
Summary: The study found that ginsenoside Rh2 can reduce the cardiotoxicity caused by doxorubicin (Dox) by inhibiting cardiac histopathological changes, apoptosis, necrosis, and inflammation. Rh2 also attenuates pathological remodeling by reducing fibroblast to myofibroblast transition (FMT) and endothelial-mesenchymal transition (EndMT). RNA-sequencing analysis showed that Dox treatment predominantly targets cell cycle and microtubule attachment, while Rh2 regulates these effects. Interestingly, Rh2 also attenuates fibrosis by promoting senescence in myofibroblasts and reversing established myofibroblast differentiation in EndMT.
CELL PROLIFERATION
(2022)
Article
Biotechnology & Applied Microbiology
Liuqin He, Xihong Zhou, Yonghui Liu, Lamei Zhou, Fengna Li
Summary: Fecal miR-142a-3p plays a role in preventing colitis by promoting the growth of Lactobacillus reuteri and alleviating disease symptoms.
Article
Biochemistry & Molecular Biology
Miao-Yi Wu, Chia-Chu Liu, Su-Chu Lee, Yueh-Hsiung Kuo, Tusty-Jiuan Hsieh
Summary: In this study, the antidiabetic activity and potential molecular mechanisms of a novel synthetic CAPE derivative (36M) were investigated using high-fat diet induced obese mouse models. The results showed that 36M prevented the progression of diabetes in the obese mice by increasing phosphorylation of AMPK and inhibiting expression of PTP1B. Additionally, 36M was found to prevent hepatic lipid storage in the mice fed with high-fat diet by inhibiting fatty acid synthase and lipid droplet proteins.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Multidisciplinary Sciences
Seung Hyun Kim, Jae Geun Lee, Hyang Mi Ju, SuYoun Choi, Hyukjin Yang, Bon-Nyeo Koo
Summary: This study aimed to compare the effects of two anesthesia methods, desflurane inhalation anesthesia and propofol-based total intravenous anesthesia (TIVA), on QT interval (QTc) values during living donor liver transplantation. The results showed that TIVA could reduce QTc prolongation compared to desflurane inhalational anesthesia, especially in patients with preoperative QTc prolongation. Additionally, patients managed with TIVA required less vasopressor during the procedure.
SCIENTIFIC REPORTS
(2022)
Article
Food Science & Technology
Jeong-Ju Lim, A-Hyun Jung, Hyung Joo Suh, Hyeon-Son Choi, Hoon Kim
Summary: This study demonstrates that LAB-P effectively prevents obesity and obesity-induced inflammatory responses caused by a high-fat diet, making it a valuable functional food ingredient for preventing obesity and treating obesity-related inflammatory diseases.
FOOD RESEARCH INTERNATIONAL
(2022)
Article
Cell Biology
Simon P. Preston, Cody C. Allison, Jan Schaefer, William Clow, Stefanie M. Bader, Sophie Collard, Wasan O. Forsyth, Michelle P. Clark, Alexandra L. Garnham, Connie S. N. Li-Wai-Suen, Thanushi Peiris, Jack Teale, Liana Mackiewicz, Sophia Davidson, Marcel Doerflinger, Marc Pellegrini
Summary: This study investigated the role of RIPK3 and MLKL in chronic LCMV infection and found that during the acute and early stages of infection, MLKL and RIPK3 did not affect the immune response and viral clearance. However, RIPK3 was found to promote immune dysfunction and prevent control of infection at later stages of chronic LCMV disease.
CELL DEATH & DISEASE
(2023)
Article
Cell Biology
Carolina Silva, Ilda Rodrigues, Sara Andrade, Raquel Costa, Raquel Soares
Summary: The study demonstrates that metformin can prevent vessel assembly in human microvascular endothelial cells through an AMPK-independent mechanism. It has an impact on the expression of key genes related to angiogenesis, while showing no significant effects on cell proliferation and invasion.
Article
Biochemistry & Molecular Biology
Laura Valles-Saiz, Jesus avila, Felix Hernandez
Summary: The dysregulation of transposable elements is involved in neurodegenerative disorders. This study investigated the protective effects of the reverse transcriptase inhibitor lamivudine in a mouse model of Alzheimer's disease. The results showed that lamivudine treatment reduced histopathological markers of tauopathies and improved motor and cognitive functions. Additional experiments revealed that tau promotes the insertion of transposable elements, and lamivudine inhibits this insertion. These findings suggest that early administration of lamivudine may attenuate the progression of tauopathies.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Genetics & Heredity
Fabien Vanden Abeele, Sabine Lotteau, Sylvie Ducreux, Charlotte Dubois, Nicole Monnier, Amy Hanna, Dimitra Gkika, Caroline Romestaing, Lucile Noyer, Matthieu Flourakis, Nolwenn Tessier, Ribal Al-Mawla, Christophe Chouabe, Etienne Lefai, Joel Lunardi, Susan Hamilton, Julien Faure, Fabien Van Coppenolle, Natalia Prevarskaya
GENETICS IN MEDICINE
(2019)
Article
Cell Biology
Tanner O. Monroe, Matthew C. Hill, Yuka Morikawa, John P. Leach, Todd Heallen, Shuyi Cao, Peter H. L. Krijger, Wouter de Laat, Xander H. T. Wehrens, George G. Rodney, James F. Martin
DEVELOPMENTAL CELL
(2019)
Article
Neurosciences
David P. Ferguson, Tanner O. Monroe, Celia Pena Heredia, Ryan Fleischmann, George G. Rodney, George E. Taffet, Marta L. Fiorotto
JOURNAL OF PHYSIOLOGY-LONDON
(2019)
Article
Multidisciplinary Sciences
Ksenia Gnedeva, Xizi Wang, Melissa M. McGovern, Matthew Barton, Litao Tao, Talon Trecek, Tanner O. Monroe, Juan Llamas, Welly Makmura, James F. Martin, Andrew K. Groves, Mark Warchol, Neil Segil
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2020)
Article
Chemistry, Multidisciplinary
Adolfo Virgen-Ortiz, Alejandro Apolinar-Iribe, Irene Diaz-Reval, Hortensia Parra-Delgado, Sarai Limon-Miranda, Enrique Alejandro Sanchez-Pastor, Luis Castro-Sanchez, Santos Jesus Castillo, Adan Dagnino-Acosta, Edgar Bonales-Alatorre, Alejandrina Rodriguez-Hernandez
Article
Multidisciplinary Sciences
Lisa K. Mullany, Aarti D. Rohira, John P. Leach, Jong H. Kim, Tanner O. Monroe, Andrea R. Ortiz, Brittany Stork, M. Waleed Gaber, Poonam Sarkar, Andrew G. Sikora, Todd K. Rosengart, Brian York, Yongcheng Song, Clifford C. Dacso, David M. Lonard, James F. Martin, Bert W. O'Malley
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2020)
Article
Multidisciplinary Sciences
Tanner O. Monroe, Melanie E. Garrett, Maria Kousi, Ramona M. Rodriguiz, Sungjin Moon, Yushi Bai, Steven C. Brodar, Karen L. Soldano, Jeremiah Savage, Thomas F. Hansen, Donna M. Muzny, Richard A. Gibbs, Lawrence Barak, Patrick F. Sullivan, Allison E. Ashley-Koch, Akira Sawa, William C. Wetsel, Thomas Werge, Nicholas Katsanis
NATURE COMMUNICATIONS
(2020)
Article
Biochemistry & Molecular Biology
Julie A. Fischer, Tanner O. Monroe, Lorenzo L. Pesce, Konrad T. Sawicki, Mattia Quattrocelli, Rosemary Bauer, Samuel D. Kearns, Matthew J. Wolf, Megan J. Puckelwartz, Elizabeth M. McNally
Summary: Genetic variation in the MTCH2 gene is associated with cardiovascular disease and metabolism, and reduction of MTCH2 may be advantageous when fatty acids are the major fuel source, but maladaptive in conditions like heart failure.
HUMAN MOLECULAR GENETICS
(2023)
Article
Physiology
Adan Dagnino-Acosta, Agustin Guerrero-Hernandez
Summary: PKC inhibitors stimulate Ca2+ release from internal stores by increasing SR Ca2+ leak mediated by translocon activation. This increased leak does not deplete the Ca2+ store, but rather compensates by increasing SERCA pump activity, leading to a new steady-state level. This change also results in increased activity of high conductance, Ca2+-sensitive potassium channels.
FRONTIERS IN PHYSIOLOGY
(2022)
Article
Physiology
Gianluigi Pironti, Stefano Gastaldello, Dilson E. Rassier, Johanna T. Lanner, Mattias Carlstrom, Lars H. Lund, Hakan Westerblad, Takashi Yamada, Daniel C. Andersson
Summary: This study used a mouse model of rheumatoid arthritis (RA) to find evidence of impaired cardiac contractile function associated with reduced Ca2+ sensitivity, increased expression of PAD2, and citrullination of alpha-actin, which was triggered by TNF-alpha. This provides molecular and physiological evidence for acquired cardiomyopathy and a potential mechanism for RA-associated heart failure.
Article
Multidisciplinary Sciences
Song Gao, Guohua Zhang, Zicheng Zhang, James Z. Zhu, Li Li, Yong Zhou, George G. Rodney Jr, Reem S. Abo-Zahrah, Lindsey Anderson, Jose M. Garcia, Yong Tae Kwon, Yi-Ping Li
Summary: Cancer induces muscle wasting through the selective degradation of myosin heavy chain subtypes IIb and IIx by the E3 ligase UBR2. Up-regulation of UBR2 by cancer leads to loss of MHC and muscle atrophy, while genetic manipulation of UBR2 levels alters MHC and muscle mass in tumor-free mice. Therapeutic interventions targeting UBR2 could potentially prevent cancer-induced muscle wasting.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2022)
Correction
Biology
James Anthony Loehr, Shang Wang, Tanya R. Cully, Rituraj Pal, Irina V. Larina, Kirill V. Larin, George G. Rodney
Editorial Material
Physiology
Arthur J. J. Cheng, Ferdinand von Walden, Johanna T. Lanner
Summary: The improvement of muscle pathology in the mdx mouse model of DMD suggests that Orai1 could be a potential drug target.
JOURNAL OF GENERAL PHYSIOLOGY
(2023)
Article
Biology
Matthew S. Penna, Rong-Chi Hu, George G. Rodney, Thomas A. Cooper
Summary: Postnatal skeletal muscle development is a highly dynamic period associated with widespread alternative splicing changes. The splicing events have implications in muscle dystrophy. LIMCH1, a stress fiber-associated protein, is spliced to generate uLIMCH1, a ubiquitously expressed isoform, and mLIMCH1, a skeletal muscle-specific isoform. mLIMCH1 knockout in mice resulted in grip strength weakness and decreased force generation. Calcium-handling deficits were observed as a mechanism for muscle weakness. LIMCH1 is mis-spliced in myotonic dystrophy type 1.
LIFE SCIENCE ALLIANCE
(2023)
Article
Biology
R. Zatarain-Palacios, S. Quijano-Scheggia, M. A. Gaytan-Hinojosa, H. Parra-Delgado, N. Salas-Marias, A. Dagnino-Acosta, S. G. Ceballos-Magana, R. Muniz-Valencia
REVISTA BIO CIENCIAS
(2020)