342 results on '"Peng, Tianqing"'
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52. Sectm1a deficiency aggravates inflammation-triggered cardiac dysfunction through disruption of LXRα signalling in macrophages
53. GDF3 Protects Mice against Sepsis-Induced Cardiac Dysfunction and Mortality by Suppression of Macrophage Pro-Inflammatory Phenotype
54. SECTM1A Positively Regulates Tissue-Resident Macrophage Self-Renewal Capacity by Boosting T Helper Cells in Mice During Endotoxemia
55. Disruption of Rac1 signaling reduces ischemia-reperfusion injury in the diabetic heart by inhibiting calpain
56. Deficiency of Rac1 Blocks NADPH Oxidase Activation, Inhibits Endoplasmic Reticulum Stress, and Reduces Myocardial Remodeling in a Mouse Model of Type 1 Diabetes
57. S-Sulfhydration of SIRT3 by Hydrogen Sulfide Attenuates Mitochondrial Dysfunction in Cisplatin-Induced Acute Kidney Injury
58. Rac1 Is Required for Cardiomyocyte Apoptosis During Hyperglycemia
59. Over-expression of calpastatin inhibits calpain activation and attenuates myocardial dysfunction during endotoxaemia
60. JNK1/c-fos inhibits cardiomyocyte TNF-α expression via a negative crosstalk with ERK and p38 MAPK in endotoxaemia
61. Disruption of phospholipase Cγ1 signalling attenuates cardiac tumor necrosis factor-α expression and improves myocardial function during endotoxemia
62. Corrigendum: Calpain activation contributes to hyperglycemia-induced apoptosis in cardiomyocytes (Cardiovascular Research (2009) 84 (100-110) DOI: 10.1093/cvr/cvp189)
63. Identifying the enzyme involved in Vacuolar ATPase acetylation during doxorubicin-induced cardiotoxicity
64. Mitochondrial ROS-induced lysosomal dysfunction impairs autophagic flux and contributes to M1 macrophage polarization in a diabetic condition
65. MicroRNA-223 is essential for maintaining functional β-cell mass during diabetes through inhibiting both FOXO1 and SOX6 pathways
66. Nicotinamide riboside promotes autolysosome clearance in preventing doxorubicin-induced cardiotoxicity
67. Tsg101 positively regulates physiologic‐like cardiac hypertrophy through FIP3‐mediated endosomal recycling of IGF‐1R
68. Calpain‐2 protects against heat stress‐induced cardiomyocyte apoptosis and heart dysfunction by blocking p38 mitogen‐activated protein kinase activation
69. Prevention of hyperglycemia-induced myocardial apoptosis by gene silencing of Toll-like receptor-4
70. Sectm1a deficiency aggravates inflammation-triggered cardiac dysfunction through disruption of LXRα signalling in macrophages.
71. Calpain Activation and Organ Failure in Sepsis: Molecular Insights and Therapeutic Perspectives
72. Circulating Exosomes Isolated from Septic Mice Induce Cardiovascular Hyperpermeability Through Promoting Podosome Cluster Formation
73. Mitochondrial calpain-1 disrupts ATP synthase and induces superoxide generation in type 1 diabetic hearts: A novel mechanism contributing to diabetic cardiomyopathy
74. Disruption of calpain reduces lipotoxicity-induced cardiac injury by preventing endoplasmic reticulum stress
75. Calpain‐2 protects against heat stress‐induced cardiomyocyte apoptosis and heart dysfunction by blocking p38 mitogen‐activated protein kinase activation.
76. Calpain-2 promotes MKP-1 expression protecting cardiomyocytes in both in vitro and in vivo mouse models of doxorubicin-induced cardiotoxicity.
77. MicroRNA-223-5p and -3p Cooperatively Suppress Necroptosis in Ischemic/Reperfused Hearts
78. Overexpression of miR-223 Tips the Balance of Pro- and Anti-hypertrophic Signaling Cascades toward Physiologic Cardiac Hypertrophy
79. Hsp20-Mediated Activation of Exosome Biogenesis in Cardiomyocytes Improves Cardiac Function and Angiogenesis in Diabetic Mice
80. Heat stress pretreatment decreases lipopolysaccharide-induced apoptosis via the p38 signaling pathway in human umbilical vein endothelial cells
81. Inhibition of MicroRNA 195 Prevents Apoptosis and Multiple-Organ Injury in Mouse Models of Sepsis
82. Abstract 13631: Therapeutic Inhibition of Mitochondrial Reactive Oxygen Species With Mito-tempo Reduces Diabetic Cardiomyopathy
83. Blockade of exosome generation with GW4869 dampens the sepsis-induced inflammation and cardiac dysfunction
84. Mitochondrial Calpain-1 Disrupts ATP Synthase and Induces Superoxide Generation in Type 1 Diabetic Hearts: A Novel Mechanism Contributing to Diabetic Cardiomyopathy
85. CIRCULATING EXOSOMES ISOLATED FROM SEPTIC MICE INDUCE CARDIOVASCULAR HYPERPERMEABILITY THROUGH PROMOTING PODOSOME CLUSTER FORMATION.
86. Exosomal miR-223 Contributes to Mesenchymal Stem Cell-Elicited Cardioprotection in Polymicrobial Sepsis
87. Deletion of capn4 Protects the Heart Against Endotoxemic Injury by Preventing ATP Synthase Disruption and Inhibiting Mitochondrial Superoxide Generation
88. Calpain-1 induces endoplasmic reticulum stress in promoting cardiomyocyte apoptosis following hypoxia/reoxygenation
89. Critical Role of Cx40 in Reduced Endothelial Electrical Coupling by Lipopolysaccharide and Hypoxia-Reoxygenation
90. Inhibition of calpain reduces oxidative stress and attenuates endothelial dysfunction in diabetes
91. Loss of duplexmiR-223 (5p and 3p) aggravates myocardial depression and mortality in polymicrobial sepsis
92. In Vivo Delivery of Adenoviral Vector Containing Interleukin-17 Receptor A Reduces Cardiac Remodeling and Improves Myocardial Function in Viral Myocarditis Leading to Dilated Cardiomyopathy
93. GW24-e2975 Over-expression of calpastatin aggravatesin vitroandin vivocardiotoxicity induced by doxorubicin
94. Enhancing Specific-Antibody Production to the ragB Vaccine with GITRL That Expand Tfh, IFN-γ+ T Cells and Attenuates Porphyromonas gingivalis Infection in Mice
95. Critical Role of Cx40 in Reduced Endothelial Electrical Coupling by Lipopolysaccharide and Hypoxia-Reoxygenation.
96. Inhibition of MicroRNA 195 Prevents Apoptosis and Multiple-Organ Injury in Mouse Models of Sepsis.
97. Mitochondrial Calpain-1 Disrupts ATP Synthase and Induces Superoxide Generation in Type 1 Diabetic Hearts: A Novel Mechanism Contributing to Diabetic Cardiomyopathy.
98. CARDIAC-SPECIFIC KNOCKOUT OF CAPN4 ATTENUATES MYOCARDIAL REMODELLING AND IMPROVES FUNCTION AFTER MYOCARDIAL INFARCTION IN MICE
99. RAC1 SIGNALLING MEDIATES DOXORUBICIN-INDUCED CARDIOTOXICITY THROUGH BOTH REACTIVE OXYGEN SPECIES DEPENDENT AND INDEPENDENT PATHWAYS
100. Rac1 signalling mediates doxorubicin-induced cardiotoxicity through both reactive oxygen species-dependent and -independent pathways
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