Neonatal Scn1b-null mice have sinoatrial node dysfunction, altered atrial structure, and atrial fibrillation.

Autor: Ramos-Mondragon R; Department of Pharmacology and., Edokobi N; Department of Pharmacology and., Hodges SL; Department of Pharmacology and., Wang S; Department of Pharmacology and., Bouza AA; Department of Pharmacology and., Canugovi C; Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA., Scheuing C; Department of Pharmacology and., Juratli L; Department of Pharmacology and., Abel WR; Department of Pharmacology and., Noujaim SF; Department of Molecular Pharmacology & Physiology, University of South Florida College of Medicine, Tampa, Florida, USA., Madamanchi NR; Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA., Runge MS; Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA., Lopez-Santiago LF; Department of Pharmacology and., Isom LL; Department of Pharmacology and.; Department of Neurology and.; Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA.

Publikováno v: JCI insight [JCI Insight] 2022 May 23; Vol. 7 (10). Date of Electronic Publication: 2022 May 23.

Human Cockayne syndrome B protein reciprocally communicates with mitochondrial proteins and promotes transcriptional elongation

Autor: Wilson, David, Berquist, BR, Canugovi, C, Sykora, P, Wilson, DM, Bohr, VA

Publikováno v: Wilson, David; Berquist, BR; Canugovi, C; Sykora, P; Wilson, DM; & Bohr, VA. (2012). Human Cockayne syndrome B protein reciprocally communicates with mitochondrial proteins and promotes transcriptional elongation.. UC San Francisco: Retrieved from: http://www.escholarship.org/uc/item/0th159fq

Cockayne syndrome (CS) is a rare human disorder characterized by pathologies of premature aging, neurological abnormalities, sensorineural hearing loss and cachectic dwarfism. With recent data identifying CS proteins as physical components of mitocho

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=od_______325::b618b497d0b79629abecd2e5fb607b05
http://www.escholarship.org/uc/item/0th159fq

N⁶ -Methyladenosine in Vascular Aging and Related Diseases: Clinical Perspectives.

Autor: Chen Li^1,2, Le Liu^1,2, Shuang Li^1,2 ls330013@csu.edu.cn, You-Shuo Liu^1,2 liuyoushuo@csu.edu.cn

Publikováno v: Aging & Disease. Aug2024, Vol. 15 Issue 4, p1447-1473. 27p.

Quercetin Attenuates KLF4-Mediated Phenotypic Switch of VSMCs to Macrophage-like Cells in Atherosclerosis: A Critical Role for the JAK2/STAT3 Pathway.

Autor: Xiang, Lu¹ (AUTHOR) xianglu66@csu.edu.cn, Wang, Yan¹ (AUTHOR), Liu, Si¹ (AUTHOR), Ying, Linyao¹ (AUTHOR), Zhang, Keyi¹ (AUTHOR), Liang, Na¹ (AUTHOR), Li, Hao¹ (AUTHOR), Luo, Gang¹ (AUTHOR) luogang@csu.edu.cn, Xiao, Lin¹ (AUTHOR) luogang@csu.edu.cn

Publikováno v: International Journal of Molecular Sciences. Jul2024, Vol. 25 Issue 14, p7755. 17p.

Increased mitochondrial NADPH oxidase 4 (NOX4) expression in aging is a causative factor in aortic stiffening.

Autor: Canugovi C; 1150 West Medical Center Drive, 7200 Medical Science Research Building III, Department of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI, 48109, USA., Stevenson MD; 1150 West Medical Center Drive, 7200 Medical Science Research Building III, Department of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI, 48109, USA., Vendrov AE; 1150 West Medical Center Drive, 7200 Medical Science Research Building III, Department of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI, 48109, USA., Hayami T; 1150 West Medical Center Drive, 7200 Medical Science Research Building III, Department of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI, 48109, USA., Robidoux J; 115 Heart Drive, Department of Pharmacology and Toxicology, The East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, 27834, North Carolina, USA., Xiao H; Institute of Vascular Medicine, Cardiology Department, Peking University Third Hospital, NHC, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, 100191, China., Zhang YY; Institute of Vascular Medicine, Cardiology Department, Peking University Third Hospital, NHC, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, 100191, China., Eitzman DT; 1150 West Medical Center Drive, 7200 Medical Science Research Building III, Department of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI, 48109, USA., Runge MS; 1150 West Medical Center Drive, 7200 Medical Science Research Building III, Department of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI, 48109, USA., Madamanchi NR; 1150 West Medical Center Drive, 7200 Medical Science Research Building III, Department of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI, 48109, USA. Electronic address: madamanc@med.umich.ediu.

Publikováno v: Redox biology [Redox Biol] 2019 Sep; Vol. 26, pp. 101288. Date of Electronic Publication: 2019 Aug 02.