Article
Multidisciplinary Sciences
Zhenzhen Chen, Qiankun He, Tiankun Lu, Jiayi Wu, Gaoli Shi, Luyun He, Hong Zong, Benyu Liu, Pingping Zhu
Summary: The study reveals that mitochondria-encoded mcPGK1 drives the mitochondrial translocation of PGK1, promoting liver tumorigenesis and TIC self-renewal by switching energy production from OXPHOS to glycolysis. This study highlights the importance of metabolic reprogramming in TICs.
NATURE COMMUNICATIONS
(2023)
Article
Biochemistry & Molecular Biology
Minji Kang, Ho Won Kim, A-Reum Yu, Jeong Seong Yang, Seung Heon Lee, Ji Won Lee, Hoe Sun Yoon, Byung Soo Lee, Hwan-Woo Park, Sung Ki Lee, Seungwan Lee, Jake Whang, Jong-Seok Kim
Summary: In this study, it was found that the rough type of Mycobacterium mucogenicum is more virulent than the smooth type, induces a stronger immune response, and leads to more extensive metabolic reprogramming. The findings provide a fundamental basis for further research on Mmuc pathogenesis.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Cell Biology
Zuzana Nahacka, Jaromir Novak, Renata Zobalova, Jiri Neuzil
Summary: Mitochondria play a crucial role in tumor cell proliferation and metastasis by facilitating adaptation to stress in the tumor microenvironment. Miro proteins are essential for regulating mitochondrial movement and distribution within cells, and they have been implicated in cancer cell migration and metastasis.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Article
Environmental Sciences
Shibo Bao, Cong Zhang, Shengxiang Luo, Liping Jiang, Qiujuan Li, Ying Kong, Jun Cao
Summary: This study reveals the important role of high mobility group A2 (HMGA2) in hexavalent chromium-induced metabolic reprogramming, shifting cellular metabolism from oxidative phosphorylation (OXPHOS) to glycolysis through the interaction of mitochondria and ER stress. The accumulation of HMGA2 proteins in mitochondria and their binding to mitochondrial DNA provide evidence for their modulation of OXPHOS.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2022)
Article
Oncology
Praveen Sharma, Vibhuti Sharma, Tarunveer Singh Ahluwalia, Nilambra Dogra, Santosh Kumar, Sandeep Singh
Summary: This study reveals that mitomiR let-7a regulates mitochondrial transcription in breast cancer cells through interaction with mtDNA, altering metabolism accordingly. These findings uncover a novel mechanism by which mitomiR plays a role in regulating mitochondrial transcription.
CANCER CELL INTERNATIONAL
(2021)
Article
Cardiac & Cardiovascular Systems
Pei-Chun Chou, Chih-Min Liu, Ching-Hui Weng, Kai-Chien Yang, Mei-Ling Cheng, Yuh-Charn Lin, Ruey-Bing Yang, Bai-Chuang Shyu, Song-Kun Shyue, Jin-Dian Liu, Shih-Pin Chen, Michael Hsiao, Yu-Feng Hu
Summary: This study reveals how fibroblasts drive the normal function of the sinoatrial node (SAN) by regulating metabolic reprogramming and rhythmic activity. The study also identifies the critical role of Aldoc in the interaction between fibroblasts and pacemaker cardiomyocytes.
CIRCULATION RESEARCH
(2022)
Article
Multidisciplinary Sciences
Eirini Lionaki, Ilias Gkikas, Ioanna Daskalaki, Maria-Konstantina Ioannidi, Maria Klapa, Nektarios Tavernarakis
Summary: Inhibition of mitochondrial protein import reduces mitochondrial abundance and extends lifespan in Caenorhabditis elegans. This effect is mediated by activation of glycolysis and de novo serine biosynthesis. The study also shows that mitochondrial chaperone induction is not essential for lifespan extension.
NATURE COMMUNICATIONS
(2022)
Review
Oncology
Yang Liu, Ruyi Xu, Huiyao Gu, Enfan Zhang, Jianwei Qu, Wen Cao, Xi Huang, Haimeng Yan, Jingsong He, Zhen Cai
Summary: Macrophages are key regulators of tissue homeostasis, involved in tissue development, repair, and defense against pathogens. TAMs play a crucial role in the tumor microenvironment, impacting tumor initiation, growth, invasion, and metastasis. The metabolic characteristics of macrophages influence their phenotype and function, with pro-inflammatory M1 macrophages relying on glycolysis and anti-inflammatory M2 macrophages more dependent on mitochondrial OXPHOS.
BIOMARKER RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Marissa D. Pokharel, David P. Marciano, Panfeng Fu, Maria Clara Franco, Hoshang Unwalla, Kim Tieu, Jeffrey R. Fineman, Ting Wang, Stephen M. Black
Summary: Mitochondria are vital for cell metabolism, growth, and function, and play a central role in endothelial cell dysfunction associated with various lung diseases, including PAH. Multiple pathways, such as nitric oxide signaling, glucose metabolism, fatty acid oxidation, and the TCA cycle, are dysregulated in PAH, leading to alterations in mitochondrial membrane potential, proliferation, and apoptosis. Further research is urgently needed, especially in endothelial cells, to fully characterize these pathways and develop effective treatments for PAH.
Article
Chemistry, Multidisciplinary
Wenjin Cai, Jinglun Zhang, Yiqian Yu, Yueqi Ni, Yan Wei, Yihong Cheng, Litian Han, Leyi Xiao, Xiaoxin Ma, Hongjiang Wei, Yaoting Ji, Yufeng Zhang
Summary: Mitochondrial transfer from macrophages to mesenchymal stem cells regulates bone homeostasis, and abnormal transfer under osteoporotic conditions leads to metabolic remodeling in stem cells.
Article
Multidisciplinary Sciences
Ratnakar Tiwari, Prashant V. Bommi, Peng Gao, Matthew J. Schipma, Yalu Zhou, Susan E. Quaggin, Navdeep S. Chandel, Pinelopi P. Kapitsinou
Summary: The impact of chemical PHD inhibition by DMOG on angiogenic competence and metabolism of human vascular ECs was investigated. The results showed that DMOG reduced cell proliferation, migration, and tube formation capacities, and led to an unfavorable metabolic reprogramming. The DMOG-induced defects in cell migration could be partially rescued by augmenting NAD(+) levels.
Review
Biochemistry & Molecular Biology
Jingjing Liu, Gaosheng Zhou, Xiaoting Wang, Dawei Liu
Summary: The importance of cell metabolism alterations during sepsis is overlooked. Metabolic reprogramming plays a crucial role in immune imbalance and organ failure associated with sepsis. It is both necessary for immune cell activation and a cause of immunosuppression. The metabolites produced by metabolic reprogramming can control the immune response. Energy shortage in sepsis leads to cell and organ dysfunction. Metabolic reprogramming can alleviate the energy crisis and enhance cell adaptation, but switching from glycolysis to OXPHOS is essential for restoring cell function.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Kelvin Pieknell, Yanuar Alan Sulistio, Noviana Wulansari, Wahyu Handoko Wibowo Darsono, Mi-Yoon Chang, Ji-Yun Ko, Jong Wook Chang, Min-Jeong Kim, Man Ryul Lee, Sang A. Lee, Hyunbeom Lee, Gakyung Lee, Byung Hwa Jung, Hyunbum Park, Geun-ho Kim, Doory Kim, Gayoung Cho, Chun-Hyung Kim, Dat Da Ly, Kyu-Sang Park, Sang-Hun Lee
Summary: Forced expression of LIN28A modulates cellular metabolism, enhancing the self-renewal and differentiation capacities of human SSCs. The metabolic reprogramming induced by LIN28A leads to improved functional capacity of mitochondria and allows for extensive cell proliferation with low levels of stress. This study provides mechanistic and practical approaches to enhance SSCs utility in regenerative medicine through LIN28A and metabolic reprogramming.
CELL DEATH AND DIFFERENTIATION
(2022)
Review
Gastroenterology & Hepatology
Chiara Raggi, Maria Letizia Taddei, Colin Rae, Chiara Braconi, Fabio Marra
Summary: Metabolic reprogramming is a characteristic of cancer, allowing tumor cells to survive and proliferate in resource-limited conditions. Cholangiocarcinoma, the second most common form of primary liver cancer, is associated with metabolic alterations such as increased aerobic glycolysis and glutamine anaplerosis. Therapeutic interventions targeting these metabolic changes may have potential benefits for treating cholangiocarcinoma.
JOURNAL OF HEPATOLOGY
(2022)
Review
Medicine, Research & Experimental
Jiajia Li, Hongmei Yang, Lingyi Zhang, Songling Zhang, Yun Dai
Summary: Cancer cells often reprogram their energy metabolism to promote growth and invasion, with oxidative phosphorylation (OXPHOS) and glycolysis playing key roles. Metabolic syndromes in women, such as obesity and hyperglycemia, increase the risk of endometrial carcinoma (EC), which is characterized by altered metabolic preferences. Targeting glycolysis and OXPHOS pathways can inhibit tumor growth and sensitize EC cells to chemotherapy. This review provides an overview of the relationship between metabolism and EC and offers insights into the development of new therapies for chemotherapy-resistant EC.
BIOMEDICINE & PHARMACOTHERAPY
(2023)