Article
Biochemistry & Molecular Biology
Giovanna Blacona, Roberto Raso, Stefano Castellani, Silvia Pierandrei, Paola Del Porto, Giampiero Ferraguti, Fiorentina Ascenzioni, Massimo Conese, Marco Lucarelli
Summary: The pathogenic mechanism of cystic fibrosis involves the interaction between the CFTR protein and the ENaC channel. By inhibiting the protease-dependent activation of ENaC and manipulating its coding genes, it is possible to reduce ENaC activity and potentially treat cystic fibrosis. The study found that inhibition of extracellular peptidases and epigenetic manipulations can effectively reduce ENaC activity, with better results in primary cells. The SCNN1B gene appears to be the most effective target for reducing ENaC activity.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2022)
Review
Cardiac & Cardiovascular Systems
Taseer Ahmad, Lale A. Ertuglu, Sepiso K. Masenga, Thomas R. Kleyman, Annet Kirabo
Summary: The d subunit of the epithelial sodium channel (ENaC) is poorly understood, but recent studies have shown its association with blood pressure, kidney function, inflammation, and salt-induced hypertension. Its expression in human vasculature and antigen presenting cells (APCs) suggests its role in vascular function and immune response.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2023)
Editorial Material
Cell Biology
Ji-Man Park, Do-Hyung Kim
Summary: In glucose-starved cells, autophagy is believed to contribute to cell survival by generating energy, with AMPK as the primary energy sensor. The current paradigm suggests that AMPK promotes autophagy by binding and phosphorylating ULK1. However, conflicting findings have cast doubt on this model. In a recent study, it was found that AMPK actually acts as a negative regulator of ULK1 activity, revealing a different role for AMPK in autophagy and its importance in cellular resilience during energy depletion.
Article
Biochemistry & Molecular Biology
Sean M. Gettings, Stephan Maxeiner, Maria Tzika, Matthew R. D. Cobain, Irina Ruf, Fritz Benseler, Nils Brose, Gabriela Krasteva-Christ, Greetje Vande Velde, Matthias Schonberger, Mike Althaus
Summary: The epithelial sodium channel (ENaC) is critical for maintaining salt and water balance in tetrapod vertebrates. While the physiology of alpha beta gamma-ENaC is well understood, the lack of mammalian model organisms has hindered research on delta beta gamma-ENaC. Recent analysis of rodent genomes revealed the presence of SCNN1D in rodents, contrary to previous beliefs, shedding light on potential new model animals for studying delta-ENaC physiology.
MOLECULAR BIOLOGY AND EVOLUTION
(2021)
Review
Cardiac & Cardiovascular Systems
Puja Paudel, Fiona J. McDonald, Martin Fronius
Summary: Delta-ENaC, the fourth subunit of vascular epithelial sodium channels, has been less understood but recent discovery of its presence in human vascular cells suggests its potential significant role in vascular physiology and pathophysiology in humans. It has different properties compared to the alpha subunit, making it a potential new drug target for cardiovascular disease treatment.
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
(2021)
Article
Multidisciplinary Sciences
Yeni Wahyuni Hartati, Dina Ratna Komala, Diana Hendrati, Shabarni Gaffar, Ari Hardianto, Yulia Sofiatin, Husein Hernandi Bahti
Summary: ENaC protein plays a crucial role in regulating sodium levels in blood plasma, and having a family history of hypertension may increase the risk of having an excessive amount of ENaC protein. An aptasensor method utilizing electrochemical techniques has been developed to detect ENaC protein levels, showing potential for urine sample testing.
ROYAL SOCIETY OPEN SCIENCE
(2021)
Article
Cell Biology
Shujie Shi, Teresa M. Buck, Andrew J. Nickerson, Jeffrey L. Brodsky, Thomas R. Kleyman
Summary: The mammalian paraoxonases (PONs) play a role in protecting against oxidative stress. Among the PON family members, PON2 and PON3 negatively regulate the expression of ENaC, an ion channel involved in salt and water balance. This study showed that PON2 functions as an ER chaperone to monitor the biogenesis of ENaC and directs the channel for ER-associated degradation, leading to reduced channel surface expression and functional activity.
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Miori Tanaka, Hirofumi Inoue, Nobuyuki Takahashi, Mariko Uehara
Summary: AMP-activated protein kinase (AMPK) serves as a crucial energy sensor in cellular metabolism and plays important roles under various metabolic stresses. This study aimed to explore the mechanistic link between AMPK and osteoclast differentiation, as well as the potential role of phytochemicals in anti-resorptive effects. The results suggest that AMPK inhibits RANKL-induced osteoclast differentiation by enhancing antioxidant defense system and regulating oxidative stress. AMPK activation by dietary-derived phytochemicals may have therapeutic potential for bone diseases.
FREE RADICAL BIOLOGY AND MEDICINE
(2023)
Article
Oncology
Adam W. Ware, Joshua J. Harris, Tania L. Slatter, Heather E. Cunliffe, Fiona J. McDonald
Summary: The study found that alpha ENaC mRNA expression is associated with breast cancer subtypes, proliferation markers, and EMT markers. Manipulating alpha ENaC expression and activity in breast cancer cells affected cell proliferation. High alpha ENaC expression was linked to less aggressive and less proliferative breast cancer subtypes, while decreased expression or activity led to increased cell proliferation in certain breast cancer cell lines.
BREAST CANCER RESEARCH AND TREATMENT
(2021)
Article
Pharmacology & Pharmacy
Jing-Wen Su, Shu-Fang Li, Jing-Jing Tao, Ya-Yun Xu, Ke Wang, Xue-Wen Qian, Ge Deng, Xiao-Qing Peng, Fei-Hu Chen
Summary: Estrogen can protect acid-induced chondrocyte injury by reducing ASIC1a protein expression, with the involvement of the autophagy-lysosome pathway and Esrra. The activation of the Esrra-AMPK-ULK1 signaling pathway by estrogen contributes to ASIC1a protein degradation and protection against acidosis-induced cytotoxicity. This study highlights the potential mechanisms by which estrogen exerts its protective effects in RA, offering insights into novel therapeutic targets for the treatment of the disease.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Matthias Worn, Hubert Kalbacher, Ferruh Artunc
Summary: This study found that urine samples from patients and mice with acute nephrotic syndrome contain specific proteolytic activity against the distal polybasic tract of γ-ENaC. This suggests the excretion of active proteases in urine or proteasuria in these individuals.
CURRENT MEDICINAL CHEMISTRY
(2022)
Article
Medicine, General & Internal
Changho Song, Yongho Lee, Shin Kim
Summary: This study found that dysregulation of ENaC-encoding genes is associated with clinicopathological features in cervical cancer patients. Overexpression of these genes may be associated with better overall survival.
INTERNATIONAL JOURNAL OF GENERAL MEDICINE
(2022)
Article
Medicine, Research & Experimental
Viktor N. Tomilin, Kyrylo Pyrshev, Anna Stavniichuk, Naghmeh Hassanzadeh Khayyat, Guohui Ren, Oleg Zaika, Sherif Khedr, Alexander Staruschenko, Fang C. Mei, Xiaodong Cheng, Oleh Pochynyuk
Summary: Epac1 and Epac2 have similar but nonredundant roles in renal sodium handling. Inhibition of Epac signaling could be instrumental in the treatment of hypertensive states associated with ENaC overactivation.
Article
Physiology
Daniel Essigke, Alexandr Ilyaskin, Matthias Woern, Bernhard N. Bohnert, Mengyun Xiao, Christoph Daniel, Kerstin Amann, Andreas L. Birkenfeld, Roman Szabo, Thomas H. Bugge, Christoph Korbmacher, Ferruh Artunc
Summary: The study aimed to explore the role of the serine protease prostasin in proteolytic ENaC activation in the kidney. Results showed that Prss8 plays a crucial role in proteolytic ENaC activation and renal function independent of its proteolytic activity.
Article
Biochemistry & Molecular Biology
Hui Li, Ning Wang, Yu Jiang, Haofei Wang, Zengfeng Xin, Huazhang An, Hao Pan, Wangqian Ma, Ting Zhang, Xiaojian Wang, Wenlong Lin
Summary: Research has identified NEDD4L as a negative regulator of inflammation signaling induced by TNF-alpha, IL-1, and IL-17. NEDD4L modulates the degradation of MEKK2 and inhibits IL-17R signaling, improving the pathogenesis of IL-17-mediated autoimmune diseases.
Article
Cell Biology
Yachen Shen, Weifeng Xu, Hui You, Dongming Su, Jing Xing, Min Li, Lei Li, Xiubin Liang
JOURNAL OF CELL SCIENCE
(2015)
Article
Cell Biology
Yanjiao Li, Yachen Shen, Min Li, Dongming Su, Weifeng Xu, Xiubin Liang, Rongshan Li
MOLECULAR AND CELLULAR BIOCHEMISTRY
(2015)
Article
Oncology
Yue-Mei Xu, Hong-Jiang Wang, Fang Chen, Wan-Hua Guo, Yan-Yang Wang, Hang-Yu Li, Jin-Hai Tang, Ying Ding, Ya-Chen Shen, Min Li, Wen-Ying Xuan, Lin-Hui Liu, Jia Wang, Xue-Rong Wang, Ze-Jun Gao, Xiu-Bin Liang, Dong-Ming Su
Article
Endocrinology & Metabolism
Weifeng Xu, Yujie Huang, Lei Li, Zhen Sun, Yachen Shen, Jing Xing, Min Li, Dongming Su, Xiubin Liang
METABOLISM-CLINICAL AND EXPERIMENTAL
(2016)
Article
Endocrinology & Metabolism
Caifeng Yan, Weifeng Xu, Yujie Huang, Min Li, Yachen Shen, Hui You, Xiubin Liang
MOLECULAR ENDOCRINOLOGY
(2016)
Article
Endocrinology & Metabolism
Yachen Shen, Hyun Cheol Roh, Manju Komori, Evan D. Rosen
MOLECULAR METABOLISM
(2017)
Article
Cell Biology
Hyun Cheol Roh, Linus T. Y. Tsai, Mengle Shao, Danielle Tenen, Yachen Shen, Manju Kumari, Anna Lyubetskaya, Christopher Jacobs, Brian Dawes, Rana K. Gupta, Evan D. Rosen
Article
Cell Biology
Lei Li, Yachen Shen, Ying Ding, Yun Liu, Dongming Su, Xiubin Liang
MOLECULAR AND CELLULAR BIOCHEMISTRY
(2014)
Article
Multidisciplinary Sciences
Lu Jia, Jing Xing, Ying Ding, Yachen Shen, Xuhui Shi, Wei Ren, Meng Wan, Jianjin Guo, Shujing Zheng, Yun Liu, Xiubin Liang, Dongming Su
Article
Cell Biology
Yachen Shen, Yvonne Su, Francisco J. Silva, Angela H. Weller, Jaimarie Sostre-Colon, Paul M. Titchenell, David J. Steger, Patrick Seale, Raymond E. Soccio
Article
Cardiac & Cardiovascular Systems
Xin Bi, Takashi Kuwano, Paul C. Lee, John S. Millar, Li Li, Yachen Shen, Raymond E. Soccio, Nicholas J. Hand, Daniel J. Rader
CIRCULATION RESEARCH
(2020)
Article
Biochemistry & Molecular Biology
Olivia Sveidahl Johansen, Tao Ma, Jakob Bondo Hansen, Lasse Kruse Markussen, Renate Schreiber, Laia Reverte-Salisa, Hua Dong, Dan Ploug Christensen, Wenfei Sun, Thorsten Gnad, Iuliia Karavaeva, Thomas Svava Nielsen, Sander Kooijman, Cheryl Cero, Oksana Dmytriyeva, Yachen Shen, Maria Razzoli, Shannon L. O'Brien, Eline N. Kuipers, Carsten Haagen Nielsen, William Orchard, Nienke Willemsen, Naja Zenius Jespersen, Morten Lundh, Elahu Gosney Sustarsic, Cecilie Morch Hallgren, Mikkel Frost, Seth McGonigle, Marie Sophie Isidor, Christa Broholm, Oluf Pedersen, Jacob Bo Hansen, Niels Grarup, Torben Hansen, Andreas Kjaer, James G. Granneman, M. Madan Babu, Davide Calebiro, Soren Nielsen, Mikael Ryden, Raymond Soccio, Patrick C. N. Rensen, Jonas Thue Treebak, Thue Walter Schwartz, Brice Emanuelli, Alessandro Bartolomucci, Alexander Pfeifer, Rudolf Zechner, Camilla Scheele, Susanne Mandrup, Zachary Gerhart-Hines
Summary: Researchers have discovered that the constitutively active receptor GPR3, through its N terminus signaling activity, induces continuous cAMP production in adipose tissue, leading to thermogenesis. Increasing GPR3 expression in thermogenic adipocytes alone is sufficient to drive energy expenditure and counteract metabolic disease.