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Specialty: Cardiology
Condition: Mitochondrial Disease

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Total 16 results found since Jan 2013.

Epigenetic modulation of Drp1-mediated mitochondrial fission by inhibition of S-adenosylhomocysteine hydrolase promotes vascular senescence and atherosclerosis
CONCLUSIONS: SAHH inhibition epigenetically upregulates Drp1 expression through repressing DNA methylation in endothelial cells, leading to vascular senescence and atherosclerosis. These results identify SAHH or SAH as a potential therapeutic target for vascular senescence and cardiovascular diseases.PMID:37517319 | DOI:10.1016/j.redox.2023.102828
Source: Atherosclerosis - July 30, 2023 Category: Cardiology Authors: Yiran You Xu Chen Yu Chen Juan Pang Qian Chen Qiannan Liu Hongliang Xue Yupeng Zeng Jinghe Xiao Jiaxin Mi Yi Tang Wenhua Ling Source Type: research

Buyang huanwu decoction inhibits diabetes-accelerated atherosclerosis via reduction of AMPK-Drp1-mitochondrial fission axis
CONCLUSION: The above findings support the conclusion that BYHWD suppresses diabetes-accelerated atherosclerosis by reducing mitochondrial fission through modulation of the AMPK/Drp1 pathway.PMID:37003404 | DOI:10.1016/j.jep.2023.116432
Source: Atherosclerosis - April 1, 2023 Category: Cardiology Authors: Wanyu Tong Ling Leng Yucheng Wang Jingwen Guo Felix Boahen Owusu Yue Zhang Fang Wang Ruiqiao Li Yuhong Li Yanxu Chang Yuefei Wang Qilong Wang Source Type: research

PCSK9 Inhibitors in Cancer Patients Treated with Immune-Checkpoint Inhibitors to Reduce Cardiovascular Events: New Frontiers in Cardioncology
Cancers (Basel). 2023 Feb 22;15(5):1397. doi: 10.3390/cancers15051397.ABSTRACTCancer patients treated with immune checkpoint inhibitors (ICIs) are exposed to a high risk of atherosclerosis and cardiometabolic diseases due to systemic inflammatory conditions and immune-related atheroma destabilization. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key protein involved in metabolism of low-density lipoprotein (LDL) cholesterol. PCSK9 blocking agents are clinically available and involve monoclonal antibodies, and SiRNA reduces LDL levels in high-risk patients and atherosclerotic cardiovascular disease events in m...
Source: Atherosclerosis - March 11, 2023 Category: Cardiology Authors: Vincenzo Quagliariello Irma Bisceglia Massimiliano Berretta Martina Iovine Maria Laura Canale Carlo Maurea Vienna Giordano Andrea Paccone Alessandro Inno Nicola Maurea Source Type: research

The enigmatic role of VCAM-1 expressed by macrophages in mitochondrial metabolism and atherosclerosis
CONCLUSION: We conclude that macrophage-specific VCAM-1 augments mitochondrial biogenesis and DNA oxidation via Cmpk2. Oxidized mitochondrial DNA in plaque macrophages increases inflammation via Sting, resulting in exacerbation of atherosclerosis.PMID:35557156 | DOI:10.1096/fasebj.2022.36.S1.R6141
Source: Atherosclerosis - May 13, 2022 Category: Cardiology Authors: Niranjana Natarajan Jonathan Florentin Scott P O'Neil Lee L Ohayon Partha Dutta Source Type: research

Salvianolic Acid B Suppresses ER Stress-Induced NLRP3 Inflammasome and Pyroptosis via the AMPK/FoxO4 and Syndecan-4/Rac1 Signaling Pathways in Human Endothelial Progenitor Cells
Oxid Med Cell Longev. 2022 Mar 17;2022:8332825. doi: 10.1155/2022/8332825. eCollection 2022.ABSTRACTMounting evidence demonstrates uncontrolled endoplasmic reticulum (ER) stress responses can activate the inflammasome, which generally results in endothelial dysfunction, a major pathogenetic factor of chronic inflammatory diseases such as atherosclerosis. Salvianolic acid B (SalB), produced by Radix Salviae, exerts antioxidative and anti-inflammatory activities in multiple cell types. However, SalB's effects on ER stress-related inflammasome and endothelial dysfunction remain unknown. Here, we showed SalB substantially abro...
Source: Atherosclerosis - March 28, 2022 Category: Cardiology Authors: Yubo Tang Qingde Wa Longyun Peng Yifan Zheng Jie Chen Xiao Chen Xuenong Zou Huangxuan Shen Shuai Huang Source Type: research

Systems Approach to Discovery of Therapeutic Targets for Vein Graft Disease PPAR α Pivotally Regulates Metabolism, Activation, and Heterogeneity of Macrophages and Lesion Development
Conclusions: This study explored potential drivers of vein graft inflammation and identified PPARα as a novel potential pharmacologic treatment for this unmet medical need.PMID:33821665 | DOI:10.1161/CIRCULATIONAHA.119.043724
Source: Circulation - April 6, 2021 Category: Cardiology Authors: Julius L Decano Sasha A Singh Cau ê Gasparotto Bueno Lang Ho Lee Arda Halu Sarvesh Chelvanambi Joan T Matamalas Hengmin Zhang Andrew K Mlynarchik Jiao Qiao Amitabh Sharma Shin Mukai Jianguo Wang Daniel G Anderson C Keith Ozaki Peter Libby Elena Aikawa Ma Source Type: research

BOLA3 Deficiency Controls Endothelial Metabolism and Glycine Homeostasis in Pulmonary Hypertension.
CONCLUSIONS: BOLA3 acts as a crucial lynchpin connecting Fe-S-dependent oxidative respiration and glycine homeostasis with endothelial metabolic re-programming critical to PH pathogenesis. These results provide a molecular explanation for the clinical associations linking PH with hyperglycinemic syndromes and mitochondrial disorders. These findings also identify novel metabolic targets, including those involved in epigenetics, iron-sulfur biogenesis, and glycine biology, for diagnostic and therapeutic development. PMID: 30759996 [PubMed - as supplied by publisher]
Source: Circulation - February 14, 2019 Category: Cardiology Authors: Yu Q, Tai YY, Tang Y, Zhao J, Negi V, Culley MK, Pilli J, Sun W, Brugger K, Mayr J, Saggar R, Saggar R, Wallace WD, Ross DJ, Waxman AB, Wendell SG, Mullett SJ, Sembrat J, Rojas M, Khan OF, Dahlman JE, Sugahara M, Kagiyama N, Satoh T, Zhang M, Feng N, Gorc Tags: Circulation Source Type: research

Metabolic Maturation of Human Pluripotent Stem Cell-Derived Cardiomyocytes by Inhibition of HIF1 α and LDHA.
CONCLUSIONS: We show that under standard culture conditions, the HIF1α-lactate dehydrogenase A axis is aberrantly upregulated in hPSC-CMs, preventing their metabolic maturation. Chemical or siRNA inhibition of this pathway results in an appropriate metabolic shift from aerobic glycolysis to oxidative phosphorylation. This in turn improves metabolic and functional maturation of hPSC-CMs. These findings provide key insight into molecular control of hPSC-CMs' metabolism and may be used to generate more physiologically mature cardiomyocytes for drug screening, disease modeling, and therapeutic purposes. PMID: 30355156 [PubMed - in process]
Source: Circulation Research - October 12, 2018 Category: Cardiology Authors: Hu D, Linders A, Yamak A, Correia C, Kijlstra JD, Garakani A, Xiao L, Milan DJ, van der Meer P, Serra M, Alves PM, Domian IJ Tags: Circ Res Source Type: research

Complex roads from genotype to phenotype in dilated cardiomyopathy: scientific update from the Working Group of Myocardial Function of the European Society of Cardiology
This article is part of the Mini Review Series from the Varenna 2017 meeting of the Working Group of Myocardial Function of the European Society of Cardiology.
Source: Cardiovascular Research - May 23, 2018 Category: Cardiology Source Type: research

Epigenetic Dysregulation of the Drp1 Binding Partners MiD49 and MiD51 Increases Mitotic Mitochondrial Fission and Promotes Pulmonary Arterial Hypertension: Mechanistic and Therapeutic Implications.
Conclusions -In health, MiDs regulate Drp1-mediated fission whilst in disease, epigenetic upregulation of MiDs increases mitotic fission, which drives pathologic proliferation and apoptosis resistance. The miR-34a-3p-MiD pathway offers new therapeutic targets for PAH. PMID: 29431643 [PubMed - as supplied by publisher]
Source: Circulation - February 5, 2018 Category: Cardiology Authors: Chen KH, Dasgupta A, Lin J, Potus F, Bonnet S, Iremonger J, Fu J, Mewburn J, Wu D, Dunham-Snary K, Theilmann AL, Jing ZC, Hindmarch C, Ormiston ML, Lawrie A, Archer SL Tags: Circulation Source Type: research

The Metabolic and Proliferative State of Vascular Adventitial Fibroblasts in Pulmonary Hypertension is Regulated through a MiR-124/PTBP1/PKM Axis.
Conclusions -In PH, miR-124, through the alternative splicing factor PTBP1, regulates the PKM2/PKM1 ratio, the overall metabolic, proliferative and inflammatory state of cells. This PH phenotype can be rescued with interventions at various levels of the metabolic cascade. These findings suggest a more integrated view of vascular cell metabolism, which may open unique therapeutic prospects in targeting the dynamic glycolytic and mitochondrial interactions and between mesenchymal inflammatory cells in PH. PMID: 28972001 [PubMed - as supplied by publisher]
Source: Circulation - September 26, 2017 Category: Cardiology Authors: Zhang H, Wang D, Li M, Plecitá-Hlavatá L, D'Alessandro A, Tauber J, Riddle S, Kumar S, Flockton AR, McKeon BA, Frid MG, Reisz JA, Caruso P, El Kasmi KC, Ježek P, Morrell NW, Hu CJ, Stenmark KR Tags: Circulation Source Type: research

MiR-21 Lowers Blood Pressure in Spontaneous Hypertensive Rats By Up-Regulating Mitochondrial Translation.
CONCLUSIONS: -Our findings reveal a positive function of miR-21 in mitochondrial translation, which is sufficient to reduce blood pressure and alleviate cardiac hypertrophy in SHRs. This observation indicates that induced miR-21 is part of the compensatory program and suggests a novel theoretical ground for developing miRNA-based therapeutics against hypertension. PMID: 27542393 [PubMed - as supplied by publisher]
Source: Circulation - August 18, 2016 Category: Cardiology Authors: Li H, Zhang X, Wang F, Zhou L, Yin Z, Fan J, Nie X, Wang P, Fu XD, Chen C, Wang D Tags: Circulation Source Type: research

Cross-talk between LOX-1 and PCSK9 in vascular tissues
Conclusions These observations suggest that LOX-1 and PCSK9 positively influence each other's expression, especially during an inflammatory reaction. mtROS appear to be important initiators of PCSK9/LOX-1 expression.
Source: Cardiovascular Research - August 18, 2015 Category: Cardiology Authors: Ding, Z., Liu, S., Wang, X., Deng, X., Fan, Y., Shahanawaz, J., Shmookler Reis, R. J., Varughese, K. I., Sawamura, T., Mehta, J. L. Tags: Vascular biology Source Type: research