azacitidine has been researched along with Ventricular Dysfunction, Left in 3 studies
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 1 (33.33) | 29.6817 |
| 2010's | 2 (66.67) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Ahn, Y; Hong, MH; Jeong, HC; Jeong, HY; Jeong, MH; Kang, WS; Kim, YS; Kwon, JS | 1 |
| Gao, XP; Gomes, I; Kishore, R; Malik, AB; Rajasingh, J; Siddiqui, MR; Thangavel, J | 1 |
| Haider, HKh | 1 |
1 review(s) available for azacitidine and Ventricular Dysfunction, Left
| Article | Year |
|---|---|
Bone marrow cells for cardiac regeneration and repair: current status and issues.
Topics: Animals; Antigens, CD34; Antimetabolites, Antineoplastic; Azacitidine; Bone Marrow Cells; Bone Marrow Transplantation; Cell Differentiation; Cell Movement; Cells, Cultured; Coronary Artery Bypass; Disease Models, Animal; Humans; Myocytes, Cardiac; Phenotype; Regeneration; Ventricular Dysfunction, Left | 2006 |
2 other study(ies) available for azacitidine and Ventricular Dysfunction, Left
| Article | Year |
|---|---|
Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis.
Topics: Animals; Antimetabolites, Antineoplastic; Azacitidine; Blotting, Western; Cells, Cultured; Fibroblasts; Fibrosis; Immunoenzyme Techniques; Macrophages; Male; Mice; Mice, Inbred BALB C; Myocardial Infarction; Nitric Oxide; Nitric Oxide Synthase; Peptidoglycan; Phenotype; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Ventricular Dysfunction, Left; Ventricular Remodeling | 2014 |
Improvement of cardiac function in mouse myocardial infarction after transplantation of epigenetically-modified bone marrow progenitor cells.
Topics: Animals; Azacitidine; Bone Marrow Cells; Cell Differentiation; Decitabine; Endothelial Cells; Epigenesis, Genetic; Gene Expression Regulation; Heart; Hydroxamic Acids; Inflammation; Male; Mice; Mice, Inbred C57BL; Myocardial Infarction; Myocytes, Cardiac; Neovascularization, Physiologic; Pluripotent Stem Cells; Stem Cell Transplantation; Stem Cells; Ventricular Dysfunction, Left | 2011 |