about
Decreased SIRT3 in aged human mesenchymal stromal/stem cells increases cellular susceptibility to oxidative stress.Phenotypic switching of vascular smooth muscle cells in the 'normal region' of aorta from atherosclerosis patients is regulated by miR-145Myometrial cells induce angiogenesis and salvage damaged myocardium.Tissue inhibitor of matrix metalloproteinase-3 or vascular endothelial growth factor transfection of aged human mesenchymal stem cells enhances cell therapy after myocardial infarction.The Expression and Related Clinical Significance of SIRT3 in Non-Small-Cell Lung Cancer.Expression of the tissue inhibitor of metalloproteinase-3 by transplanted VSMCs modifies heart structure and function after myocardial infarction.Reduced ischemic injury after stroke in mice by angiogenic gene delivery via ultrasound-targeted microbubble destruction.Inhibiting matrix metalloproteinase by cell-based timp-3 gene transfer effectively treats acute and chronic ischemic cardiomyopathy.Combined treatment with simvastatin and rapamycin attenuates cardiac allograft rejection through the regulation of T helper 17 and regulatory T cells.Suppression of miR-34a Expression in the Myocardium Protects Against Ischemia-Reperfusion Injury Through SIRT1 Protective Pathway.Lower Senescence of Adipose-Derived Stem Cells than Donor-Matched Bone Marrow Stem Cells for Surgical Ventricular Restoration.TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction.Sirtuin3 protects aged human mesenchymal stem cells against oxidative stress and enhances efficacy of cell therapy for ischaemic heart diseasesThe microRNA-328 regulates hypoxic pulmonary hypertension by targeting at insulin growth factor 1 receptor and L-type calcium channel-α1CExpression of ADAM-15 in rat myocardial infarction[Enhancement of gene transfection efficiency and therapeutic effect of ultrasound-targeted microbubble destruction in vivo with cationic microbubble]
P50
Q34473688-D3CC063D-35B2-446C-B6D7-388DECE8E65CQ36942350-D2FDFF41-1DBA-4D3C-926C-87705719CD36Q38483643-AE583760-DD94-4184-91CE-259836C7ED74Q41672067-08C837EC-E797-4FE7-8BCD-59D4250E42F7Q41691894-1F9EA1D8-5030-41D3-904E-624EA2B69F77Q45864109-3CE1E691-D21D-425D-9CB6-5C8FB2E7B5B7Q45864924-8FB3A212-2098-460F-A884-7AFE94FC90D9Q45873510-5F6AF475-87BA-41B0-A0F2-A6ADA21F8F12Q49477710-4B708AF2-3DCB-42D3-810A-07A5582D0FDCQ50951747-082FDFF5-DF1C-4FDA-81A0-A0D46ED7414EQ52720690-193330EF-4D2E-472F-A3FE-664BF7EE8BA7Q53521178-5543751A-53C8-4BB4-ACE3-66B5BDA4D344Q58791789-0DC6E7DD-579E-4193-9B98-BE1DBAAD0DA8Q83578490-2FD924D7-F21B-4917-AF7F-1FEB994D079AQ84140281-70EAD562-1144-4E2D-B637-478D16C46912Q88880234-9468932B-9342-4B6E-8A34-451754F65E3B
P50
description
researcher ORCID ID = 0000-0001-9127-3511
@en
wetenschapper
@nl
name
Hai Tian
@ast
Hai Tian
@en
Hai Tian
@es
Hai Tian
@nl
type
label
Hai Tian
@ast
Hai Tian
@en
Hai Tian
@es
Hai Tian
@nl
prefLabel
Hai Tian
@ast
Hai Tian
@en
Hai Tian
@es
Hai Tian
@nl
P1153
36742815200
P31
P496
0000-0001-9127-3511