Xian-Liang Tang

Nitric oxide donors induce late preconditioning against myocardial stunning and infarction in conscious rabbits via an antioxidant-sensitive mechanism.

Demonstration of an early and a late phase of ischemic preconditioning in mice.

The late phase of ischemic preconditioning is abrogated by targeted disruption of the inducible NO synthase gene.

Cyclooxygenase-2 mediates the cardioprotective effects of the late phase of ischemic preconditioning in conscious rabbits.

Evidence for an essential role of cyclooxygenase-2 as a mediator of the late phase of ischemic preconditioning in mice.

Gene therapy with extracellular superoxide dismutase protects conscious rabbits against myocardial infarction.

Oxidant species trigger late preconditioning against myocardial stunning in conscious rabbits.

Nitric oxide (NO) induces nitration of protein kinase Cepsilon (PKCepsilon ), facilitating PKCepsilon translocation via enhanced PKCepsilon -RACK2 interactions: a novel mechanism of no-triggered activation of PKCepsilon.

Formation of protein kinase C(epsilon)-Lck signaling modules confers cardioprotection.

Inducible nitric oxide synthase modulates cyclooxygenase-2 activity in the heart of conscious rabbits during the late phase of ischemic preconditioning.

Role of cyclic guanosine monophosphate in late preconditioning in conscious rabbits.

Role of Src protein tyrosine kinases in late preconditioning against myocardial infarction.

Discovery of a new function of cyclooxygenase (COX)-2: COX-2 is a cardioprotective protein that alleviates ischemia/reperfusion injury and mediates the late phase of preconditioning.

Aldose reductase is an obligatory mediator of the late phase of ischemic preconditioning.

Delta-opioid receptor-induced late preconditioning is mediated by cyclooxygenase-2 in conscious rabbits.

Protein tyrosine kinase signaling is necessary for NO donor-induced late preconditioning against myocardial stunning.

Effect of aspirin on late preconditioning against myocardial stunning in conscious rabbits.

Nonelectrocardiographic evidence that both ischemic preconditioning and adenosine preconditioning exist in humans.

Nicorandil induces late preconditioning against myocardial infarction in conscious rabbits.

Cardioprotection during the final stage of the late phase of ischemic preconditioning is mediated by neuronal NO synthase in concert with cyclooxygenase-2.

Hypercholesterolemia blunts NO donor-induced late preconditioning against myocardial infarction in conscious rabbits.

Delayed adaptation of the heart to stress: late preconditioning.

Cardiac stem cells delivered intravascularly traverse the vessel barrier, regenerate infarcted myocardium, and improve cardiac function.

Delayed preconditioning-mimetic actions of nitroglycerin in patients undergoing exercise tolerance tests.

Hypercholesterolemia abrogates late preconditioning via a tetrahydrobiopterin-dependent mechanism in conscious rabbits.

Redox activation of aldose reductase in the ischemic heart.

Cardioprotection by postconditioning in conscious rats is limited to coronary occlusions <45 min.

Effects of anesthesia on echocardiographic assessment of left ventricular structure and function in rats.

Pretreatment with intracoronary enalaprilat protects human myocardium during percutaneous coronary angioplasty.

The late phase of preconditioning and its natural clinical application--gene therapy.

The cardioprotection of the late phase of ischemic preconditioning is enhanced by postconditioning via a COX-2-mediated mechanism in conscious rats.

Role of nitric oxide in regulating aldose reductase activation in the ischemic heart.

Noncanonical Wnt11 signaling is sufficient to induce cardiomyogenic differentiation in unfractionated bone marrow mononuclear cells.

The role of TNF-alpha receptors p55 and p75 in acute myocardial ischemia/reperfusion injury and late preconditioning.

Intracoronary administration of cardiac progenitor cells alleviates left ventricular dysfunction in rats with a 30-day-old infarction.

Cardiac progenitor cells and bone marrow-derived very small embryonic-like stem cells for cardiac repair after myocardial infarction.

Transplantation of expanded bone marrow-derived very small embryonic-like stem cells (VSEL-SCs) improves left ventricular function and remodelling after myocardial infarction.

Atorvastatin therapy during the peri-infarct period attenuates left ventricular dysfunction and remodeling after myocardial infarction.

The heme oxygenase 1 inducer (CoPP) protects human cardiac stem cells against apoptosis through activation of the extracellular signal-regulated kinase (ERK)/NRF2 signaling pathway and cytokine release.

Intracoronary delivery of autologous cardiac stem cells improves cardiac function in a porcine model of chronic ischemic cardiomyopathy.

Cardiac myocyte-specific transgenic ecSOD targets mitochondria to protect against Ca(2+) induced permeability transition.

The NHLBI-sponsored Consortium for preclinicAl assESsment of cARdioprotective therapies (CAESAR): a new paradigm for rigorous, accurate, and reproducible evaluation of putative infarct-sparing interventions in mice, rabbits, and pigs.

Safety of intracoronary infusion of 20 million C-kit positive human cardiac stem cells in pigs.

Effects of Intracoronary Infusion of Escalating Doses of Cardiac Stem Cells in Rats With Acute Myocardial Infarction.

Effect of the stop-flow technique on cardiac retention of c-kit positive human cardiac stem cells after intracoronary infusion in a porcine model of chronic ischemic cardiomyopathy.

Long-Term Outcome of Administration of c-kit(POS) Cardiac Progenitor Cells After Acute Myocardial Infarction: Transplanted Cells Do not Become Cardiomyocytes, but Structural and Functional Improvement and Proliferation of Endogenous Cells Persist for at Least One Year.

Repeated Administrations of Cardiac Progenitor Cells Are Markedly More Effective Than a Single Administration: A New Paradigm in Cell Therapy.

Myocardial Reparative Properties of Cardiac Mesenchymal Cells Isolated on the Basis of Adherence.

Repeated Administrations of Cardiac Progenitor Cells Are Superior to a Single Administration of an Equivalent Cumulative Dose.

Epigenetically modified cardiac mesenchymal stromal cells limit myocardial fibrosis and promote functional recovery in a model of chronic ischemic cardiomyopathy.

Physiological Biomimetic Culture System for Pig and Human Heart Slices.

The Effect of Cardiogenic Factors on Cardiac Mesenchymal Cell Anti-Fibrogenic Paracrine Signaling and Therapeutic Performance.