Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice - Wikidata - awgldk - TriplyDB

Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice

Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice

http://www.wikidata.org/entity/Q36404982

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Heart failure with preserved ejection fraction: emerging drug strategies The circular relationship between matrix metalloproteinase-9 and inflammation following myocardial infarction Role of estrogen in diastolic dysfunction Age-associated pro-inflammatory remodeling and functional phenotype in the heart and large arteries Quality control systems in cardiac aging Diastolic dysfunction Cardiac aging is initiated by matrix metalloproteinase-9-mediated endothelial dysfunction.Age-related changes in tissue macrophages precede cardiac functional impairment Farnesoid X receptor deletion improves cardiac function, structure and remodeling following myocardial infarction in mice Multifaceted Roles of Metzincins in CNS Physiology and Pathology: From Synaptic Plasticity and Cognition to Neurodegenerative Disorders And the beat goes on: maintained cardiovascular function during aging in the longest-lived rodent, the naked mole-rat.Salvianolic acid A, a novel matrix metalloproteinase-9 inhibitor, prevents cardiac remodeling in spontaneously hypertensive rats.The dopamine D3 receptor knockout mouse mimics aging-related changes in autonomic function and cardiac fibrosis Secreted protein acidic and rich in cysteine facilitates age-related cardiac inflammation and macrophage M1 polarization.Deriving a cardiac ageing signature to reveal MMP-9-dependent inflammatory signalling in senescence.Resveratrol ameliorates myocardial fibrosis by inhibiting ROS/ERK/TGF-β/periostin pathway in STZ-induced diabetic mice.Ataxia telangiectasia-mutated kinase deficiency exacerbates left ventricular dysfunction and remodeling late after myocardial infarction Tissue Inhibitor of Metalloproteinase-1: Actions beyond Matrix Metalloproteinase Inhibition.Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling Low-Dose and Short-Duration Matrix Metalloproteinase 9 Inhibition Does Not Affect Adhesion Formation during Murine Flexor Tendon Healing.Ablation of Matrix Metalloproteinase-9 Prevents Cardiomyocytes Contractile Dysfunction in Diabetics Aberrant differentiation of fibroblast progenitors contributes to fibrosis in the aged murine heart: role of elevated circulating insulin levels.Mechanical Regulation of Cardiac Aging in Model Systems.Pharmacological Strategies to Retard Cardiovascular Aging Matrix metalloproteinase-9-dependent mechanisms of reduced contractility and increased stiffness in the aging heart Using the laws of thermodynamics to understand how matrix metalloproteinases coordinate the myocardial response to injury Increased ADAMTS1 mediates SPARC-dependent collagen deposition in the aging myocardium.Aging and the cardiac collagen matrix: Novel mediators of fibrotic remodelling Myocardial Infarction Superimposed on Aging: MMP-9 Deletion Promotes M2 Macrophage Polarization.Lack of ABCG2 Leads to Biventricular Dysfunction and Remodeling in Response to Hypoxia Age and SPARC change the extracellular matrix composition of the left ventricle.Investigational drugs targeting cardiac fibrosis.Cardiac Physiology of Aging: Extracellular Considerations.Cardiac extracellular matrix proteomics: Challenges, techniques, and clinical implications The Aging Heart Association between vitamin D deficiency and heart failure risk in the elderly.Management of Heart Failure with Preserved Ejection Fraction: Current Challenges and Future Directions.Cardiac fibrosis in the ageing heart: contributors and mechanisms.Complex IV-deficient Surf1(-/-) mice initiate mitochondrial stress responses.Characterization of age-related penile microvascular hemodynamic impairment using laser speckle contrast imaging: possible role of increased fibrogenesis.

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Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice

http://www.wikidata.org/entity/Q36404982

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Jianhua Zhang

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Merry L Lindsey

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Qiuxia Dai

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S Michelle Okoronkwo

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Trevi A Ramirez

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Ying Ann Chiao

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Yu-Fang Jin

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Cell surface-localized matrix metalloproteinase-9 proteolytically activates TGF-beta and promotes tumor invasion and angiogenesis

MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes

TGF-beta signalling from cell membrane to nucleus through SMAD proteins

The collagen substrate specificity of human neutrophil collagenase

Periostin as a novel factor responsible for ventricular dilation

Connective tissue growth factor overexpression in cardiomyocytes promotes cardiac hypertrophy and protection against pressure overload

Angiotensin II increases periostin expression via Ras/p38 MAPK/CREB and ERK1/2/TGF-β1 pathways in cardiac fibroblasts

New functions for the matrix metalloproteinases in cancer progression

How matrix metalloproteinases regulate cell behavior

Involvement of NADPH oxidase in age-associated cardiac remodeling

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10.1093/CVR/CVS275

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