Page last updated: 2024-08-22

hyaluronoglucosaminidase and Ventricular Dysfunction, Left

hyaluronoglucosaminidase has been researched along with Ventricular Dysfunction, Left in 2 studies

Research

Studies (2)

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	0 (0.00)	29.6817
2010's	1 (50.00)	24.3611
2020's	1 (50.00)	2.80

Authors

Authors	Studies
Chatham, JC; Davey, JR; Davidoff, AJ; De Blasio, MJ; Deo, M; Donner, DG; Erickson, JR; Gregorevic, P; Henstridge, DC; Kiriazis, H; Lees, JG; Lim, SY; Parry, LJ; Prakoso, D; Qian, H; Ritchie, RH; Tate, M; Wallace, RS	1
Chowdhury, B; Dolinsky, VW; Hemming, R; Liu, M; Triggs-Raine, B; Xiang, B	1

Other Studies

2 other study(ies) available for hyaluronoglucosaminidase and Ventricular Dysfunction, Left

Article	Year
Fine-tuning the cardiac O-GlcNAcylation regulatory enzymes governs the functional and structural phenotype of the diabetic heart. Cardiovascular research, 2022, 01-07, Volume: 118, Issue:1 Topics: Aged; Animals; Antigens, Neoplasm; Cell Line; Class I Phosphatidylinositol 3-Kinases; Diabetic Cardiomyopathies; Disease Models, Animal; Female; Fibrosis; Gene Expression Regulation; Glycosylation; Histone Acetyltransferases; Humans; Hyaluronoglucosaminidase; Male; Mice; Middle Aged; Myocytes, Cardiac; N-Acetylglucosaminyltransferases; Phenotype; Protein Processing, Post-Translational; Proto-Oncogene Proteins c-akt; Reactive Oxygen Species; Signal Transduction; Ventricular Dysfunction, Left; Ventricular Function, Left; Ventricular Remodeling	2022
Hyaluronidase 2 Deficiency Causes Increased Mesenchymal Cells, Congenital Heart Defects, and Heart Failure. Circulation. Cardiovascular genetics, 2017, Volume: 10, Issue:1 Topics: Animals; Cardiomegaly; Cell Proliferation; Disease Progression; Endothelial Cells; Epithelial-Mesenchymal Transition; Fibrosis; Genetic Predisposition to Disease; GPI-Linked Proteins; Heart Defects, Congenital; Heart Failure; Heart Valve Diseases; Hyaluronic Acid; Hyaluronoglucosaminidase; Mesenchymal Stem Cells; Mice, Inbred C57BL; Mice, Knockout; Myocardial Contraction; Phenotype; Stroke Volume; Time Factors; Ventricular Dysfunction, Left; Ventricular Function, Left	2017

Article

Year

Fine-tuning the cardiac O-GlcNAcylation regulatory enzymes governs the functional and structural phenotype of the diabetic heart.

Cardiovascular research, 2022, 01-07, Volume: 118, Issue:1

Topics: Aged; Animals; Antigens, Neoplasm; Cell Line; Class I Phosphatidylinositol 3-Kinases; Diabetic Cardiomyopathies; Disease Models, Animal; Female; Fibrosis; Gene Expression Regulation; Glycosylation; Histone Acetyltransferases; Humans; Hyaluronoglucosaminidase; Male; Mice; Middle Aged; Myocytes, Cardiac; N-Acetylglucosaminyltransferases; Phenotype; Protein Processing, Post-Translational; Proto-Oncogene Proteins c-akt; Reactive Oxygen Species; Signal Transduction; Ventricular Dysfunction, Left; Ventricular Function, Left; Ventricular Remodeling

2022

Hyaluronidase 2 Deficiency Causes Increased Mesenchymal Cells, Congenital Heart Defects, and Heart Failure.

Circulation. Cardiovascular genetics, 2017, Volume: 10, Issue:1

Topics: Animals; Cardiomegaly; Cell Proliferation; Disease Progression; Endothelial Cells; Epithelial-Mesenchymal Transition; Fibrosis; Genetic Predisposition to Disease; GPI-Linked Proteins; Heart Defects, Congenital; Heart Failure; Heart Valve Diseases; Hyaluronic Acid; Hyaluronoglucosaminidase; Mesenchymal Stem Cells; Mice, Inbred C57BL; Mice, Knockout; Myocardial Contraction; Phenotype; Stroke Volume; Time Factors; Ventricular Dysfunction, Left; Ventricular Function, Left

2017