Article
Biochemistry & Molecular Biology
Hanna Sarah Kutsche, Rolf Schreckenberg, Klaus-Dieter Schlueter
Summary: Uncoupling proteins UCP2 and UCP3 may have multiple functions in striated muscles, including protection against mitochondria-dependent oxidative stress, transportation of pyruvate, fatty acids, and protons, and metabolic sensing. UCP2 is mainly expressed in cardiac tissues, while UCP3 dominates in skeletal muscles.
ANTIOXIDANTS & REDOX SIGNALING
(2022)
Review
Geriatrics & Gerontology
Lu Zou, Yanyan Yang, Zhibin Wang, Xiuxiu Fu, Xiangqin He, Jiayi Song, Tianxiang Li, Huibo Ma, Tao Yu
Summary: Malonylation is a recently discovered post-translational modification with broad significance in both prokaryotes and eukaryotes. Recent advancements in bioinformatic analysis have enhanced our understanding of its role in protein regulation and its involvement in various biological processes. This review summarizes the theory and mechanism of malonylation, highlights recent progress, and explores its potential applications in disease diagnosis and therapy.
Article
Endocrinology & Metabolism
Jing Luo, Yao Wang, Elizabeth Gilbert, Dongmin Liu
Summary: Deletion of GPR30 protects female mice from HFD-induced obesity by regulating energy metabolism and adipocyte differentiation.
FRONTIERS IN ENDOCRINOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Linmeng Han, Chunyu Zhang, Danni Wang, Jiaqi Zhang, Qiqi Tang, Mulin Jun Li, Michael N. Sack, Lingdi Wang, Lu Zhu
Summary: Metabolic reprogram is crucial for cancer cell growth and movement, and mitochondrial protein acetylation plays a role in regulating mitochondrial metabolism and cancer cell migration. This study shows that the loss of regulator GCN5L1 promotes reactive oxygen species generation and enhances fatty acid oxidation, leading to mitochondrial fission and cell migration in hepatocellular carcinoma (HCC). Increased acetyl-CoA levels, a product of fatty acid oxidation, also enhance HCC cell migration. These findings highlight the importance of GCN5L1 and fatty acid oxidation in HCC metastasis.
Article
Chemistry, Multidisciplinary
Jia-Zih Dai, Yen-Ju Wang, Cheng-Hsun Chen, I-Lin Tsai, Yi-Chun Chao, Cheng-Wei Lin
Summary: Hormone dysregulation is considered a risk factor for obesity-mediated breast tumorigenesis. However, obesity is associated with poor outcomes among women diagnosed with hormone-independent breast cancer subtype called triple-negative breast cancer (TNBC). This study found that diet-induced obesity (DIO) facilitates tumorigenesis of TNBC cells. Mechanistically, DIO induces a metabolic addiction to fatty acid oxidation (FAO) and activates Yes-associated protein (YAP) signaling. YAP regulates mitochondrial redox homeostasis through transcriptional regulation of antioxidant-related enzymes, therefore protecting tumor cells from FAO-induced mitochondrial oxidative stress. Adipocytes-derived fatty acids are responsible for enhancing the FAO-YAP axis and antioxidative capacity. Additionally, higher expression of an obesity signature in breast cancer patients is positively correlated with YAP signaling and antioxidant genes. The findings reveal the crucial role of YAP in dictating mitochondrial redox homeostasis for obesity-mediated metabolic adaptation and breast tumor progression.
Article
Biochemistry & Molecular Biology
Yi Wu, Keshi Chen, Linpeng Li, Zhihong Hao, Tianyu Wang, Yang Liu, Guangsuo Xing, Zichao Liu, Heying Li, Hao Yuan, Jianghuan Lu, Cheng Zhang, Jinye Zhang, Danyun Zhao, Junwei Wang, Jinfu Nie, Dan Ye, Guangjin Pan, Wai-Yee Chan, Xingguo Liu
Summary: This study reveals the critical role of Plin2-mediated lipid hydrolysis in embryonic stem cell pluripotency. The degradation of Plin2 facilitates lipid droplet mobilization, and excessive lipid hydrolysis leads to lipidomic remodeling, defects in mitochondrial structure and fatty acid oxidation, resulting in the loss of pluripotency.
CELL DEATH AND DIFFERENTIATION
(2022)
Review
Cell Biology
Teresa Campbell, Jesse Slone, Taosheng Huang
Summary: Mitochondria, responsible for generating energy in the form of ATP, have their own genetic material called mtDNA, along with nuclear genome, that determines their structure and function. Pathogenic variants in mtDNA or nuclear genome can cause mitochondrial disease, especially affecting high energy-demanding tissues like the heart. Mitochondrial cardiomyopathy, a result of genetic defects in either nDNA or mtDNA, manifests as hypertrophic or dilated cardiomyopathy and cardiac conduction defects. The complex pathophysiology of mitochondrial cardiomyopathy involves various abnormal processes such as deficient oxidative phosphorylation, ATP depletion, activation of alternative metabolic pathways, accumulation of reactive oxygen species, dysfunctional mitochondrial dynamics, abnormal calcium homeostasis, and mitochondrial iron overload.
Article
Immunology
Priscila Camillo Teixeira, Axel Ducret, Hanno Langen, Everson Nogoceke, Ronaldo Honorato Barros Santos, Joao Paulo Silva Nunes, Luiz Benvenuti, Debora Levy, Sergio Paulo Bydlowski, Edimar Alcides Bocchi, Andreia Kuramoto Takara, Alfredo Inacio Fiorelli, Noedir Antonio Stolf, Pablo Pomeranzeff, Christophe Chevillard, Jorge Kalil, Edecio Cunha-Neto
Summary: Proteomic study in myocardial tissue samples from CCC, IC and DCM revealed altered expression of proteins related to mitochondrial energy metabolism, cardiac remodeling, and oxidative stress. CCC patients' myocardium displayed reduced expression of 22 mitochondrial proteins belonging to energy metabolism pathways, emphasizing a major reduction of mitochondrial energy metabolism in CCC.
FRONTIERS IN IMMUNOLOGY
(2021)
Review
Immunology
Yen-Ju Lin, Alexandra Goretzki, Stefan Schuelke
Summary: Allergic disorders have been on the rise in recent decades, prompting the emergence of a new research field called immune metabolism. It has been found that metabolic changes in T and B cells may play a role in the development and maintenance of allergies.
FRONTIERS IN IMMUNOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Jan Haas, Karen S. Frese, Farbod Sedaghat-Hamedani, Elham Kayvanpour, Rewati Tappu, Rouven Nietsch, Oguz Firat Tugrul, Michael Wisdom, Carsten Dietrich, Ali Amr, Tanja Weis, Torsten Niederdraenk, Michael P. Murphy, Thomas Krieg, Marcus Doerr, Uwe Voelker, Jens Fielitz, Norbert Frey, Stephan B. Felix, Andreas Keller, Hugo A. Katus, Benjamin Meder
Summary: This study identified a new set of metabolomic biomarkers for heart failure (HF) through a multi-OMICS approach, revealing underlying biological cascades that potentially represent suitable intervention targets.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Biochemistry & Molecular Biology
Mariana Fernandez-Caggiano, Philip Eaton
Summary: The mitochondrial pyruvate carrier (MPC) plays a crucial role in determining the fate of pyruvate in cells, with decreased expression contributing to lactate accumulation in the cytosol. Reduced MPC abundance has also been observed in failing hearts, suggesting a potential causal role in heart failure progression.
CELL DEATH AND DIFFERENTIATION
(2021)
Article
Biochemistry & Molecular Biology
Sanja Skulj, Zlatko Brkljaca, Jurgen Kreiter, Elena E. Pohl, Mario Vazdar
Summary: Molecular dynamics simulations of uncoupling proteins present a challenge due to the lack of available structural data. In this study, a combination of homology modelling and MD simulations of UCP2 revealed a structure impermeable to water. Additionally, results from conductance measurements in model membranes suggest that the UCP2 structure modeled from ANT protein possesses key functional elements related to proton transport.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Oncology
Haowen Jiang, Rachel L. Greathouse, Sarah Jane Tiche, Man Zhao, Bo He, Yang Li, Albert M. Li, Balint Forgo, Michaela Yip, Allison Li, Moriah Shih, Selene Banuelos, Meng-Ning Zhou, Joshua J. Gruber, Erinn B. Rankin, Zhen Hu, Hiroyuki Shimada, Bill Chiu, Jiangbin Ye
Summary: The Warburg effect is the major metabolic hallmark of cancer. In this study, researchers found that treating neuroblastoma cells with the mitochondrial uncoupler NEN can induce neural differentiation by altering metabolic and epigenetic pathways.
Article
Chemistry, Multidisciplinary
Haiyan Chen, Wendan Pu, Xiankang Hu, Cheng Yang, Guanli Zhao, Houyuan Hu, Jianxiang Zhang
Summary: This article reports a mitochondrial-mimetic therapy for dilated cardiomyopathy (DCM) that efficiently targets the heart, cardiomyocytes, and myocardial mitochondria, effectively regulating mitochondrial homeostasis. By synthesizing a bioactive conjugate TPT and delivering it intravenously, TPTN can accumulate in the heart and primarily localize in the cardiomyocytes and myocardial mitochondria, alleviating DCM. By packaging TPTN into outer mitochondrial membrane-derived vesicles, a mitochondrial-mimetic therapy with enhanced targeting capability is created, providing notable therapeutic effects in DCM mice.
ADVANCED FUNCTIONAL MATERIALS
(2023)
Review
Biochemistry & Molecular Biology
Siarhei A. Dabravolski, Evgeny E. Bezsonov, Mirza S. Baig, Tatyana V. Popkova, Alexander N. Orekhov
Summary: The prevalence of NAFLD is rapidly increasing globally, with cardiovascular diseases being the most common cause of mortality in NAFLD patients. Atherogenic dyslipidemia, altered fatty-acid beta-oxidation in liver mitochondria, and various NAFLD-associated genes with cardioprotective effects are key factors connecting NAFLD-mediated dyslipidemia and increased cardiovascular disease risk.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)