Interleukin-9 aggravates doxorubicin-induced cardiotoxicity by promoting inflammation and apoptosis in mice.
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Jianfang Liu | Jing Ye | Zhen Wang | Menglong Wang | Yao Xu | Di Ye | J. Wan | Jiangbin Chen | Jishou Zhang | Mengmeng Zhao
[1] Jie Jiang,et al. Costunolide enhances sensitivity of K562/ADR chronic myeloid leukemia cells to doxorubicin through PI3K/Akt pathway , 2019, Phytotherapy research : PTR.
[2] A. Ihsan,et al. Chitosan oligosaccharides prevent doxorubicin-induced oxidative stress and cardiac apoptosis through activating p38 and JNK MAPK mediated Nrf2/ARE pathway. , 2019, Chemico-biological interactions.
[3] D. Mitra,et al. An Update on Interleukin-9: From Its Cellular Source and Signal Transduction to Its Role in Immunopathogenesis , 2019, International journal of molecular sciences.
[4] Zou Sc,et al. IL-9 exacerbates the development of chronic obstructive pulmonary disease through oxidative stress. , 2018 .
[5] N. Yusuf,et al. Doxorubicin triggers splenic contraction and irreversible dysregulation of COX and LOX that alters the inflammation-resolution program in the myocardium. , 2018, American journal of physiology. Heart and circulatory physiology.
[6] F. Zhu,et al. IL-9 Promotes the Development of Deep Venous Thrombosis by Facilitating Platelet Function , 2018, Thrombosis and Haemostasis.
[7] Ji-fan Hu,et al. Cytokine IL9 Triggers the Pathogenesis of Inflammatory Bowel Disease Through the miR21-CLDN8 Pathway. , 2018, Inflammatory bowel diseases.
[8] Jing Ye,et al. Circulating Th1, Th2, Th9, Th17, Th22, and Treg Levels in Aortic Dissection Patients , 2018, Mediators of inflammation.
[9] Jianfang Liu,et al. Interleukin-12p35 Knock Out Aggravates Doxorubicin-Induced Cardiac Injury and Dysfunction by Aggravating the Inflammatory Response, Oxidative Stress, Apoptosis and Autophagy in Mice , 2018, EBioMedicine.
[10] A. Angelini,et al. Phosphoinositide 3-Kinase Gamma Inhibition Protects From Anthracycline Cardiotoxicity and Reduces Tumor Growth , 2018, Circulation.
[11] Jianfang Liu,et al. Inhibition of TRPA1 Attenuates Doxorubicin-Induced Acute Cardiotoxicity by Suppressing Oxidative Stress, the Inflammatory Response, and Endoplasmic Reticulum Stress , 2018, Oxidative medicine and cellular longevity.
[12] N. Hadi,et al. Enoxaparin attenuates doxorubicin induced cardiotoxicity in rats via interfering with oxidative stress, inflammation and apoptosis , 2018, BMC Pharmacology and Toxicology.
[13] Jun Ren,et al. Rutin attenuates doxorubicin-induced cardiotoxicity via regulating autophagy and apoptosis. , 2017, Biochimica et biophysica acta. Molecular basis of disease.
[14] M. Neurath,et al. Resolution of inflammation by interleukin-9-producing type 2 innate lymphoid cells , 2017, Nature Medicine.
[15] J. Wu,et al. Gp130-mediated STAT3 activation by S-propargyl-cysteine, an endogenous hydrogen sulfide initiator, prevents doxorubicin-induced cardiotoxicity , 2016, Cell Death and Disease.
[16] F. Giallauria,et al. Detectable interleukin-9 plasma levels are associated with impaired cardiopulmonary functional capacity and all-cause mortality in patients with chronic heart failure. , 2016, International journal of cardiology.
[17] S. Raychaudhuri,et al. IL-9, a local growth factor for synovial T cells in inflammatory arthritis. , 2016, Cytokine.
[18] M. Ciccarelli,et al. Inflammatory mediators in a short-time mouse model of doxorubicin-induced cardiotoxicity. , 2016, Toxicology and applied pharmacology.
[19] S. Wen,et al. IL-9 aggravates the development of atherosclerosis in ApoE-/- mice. , 2015, Cardiovascular research.
[20] Kenji Suzuki,et al. Myocardial 14-3-3η protein protects against mitochondria mediated apoptosis. , 2015, Cellular signalling.
[21] M. Neurath,et al. IL-9 regulates intestinal barrier function in experimental T cell-mediated colitis , 2015, Tissue barriers.
[22] Hulun Li,et al. Neutralization of interleukin‐9 ameliorates symptoms of experimental autoimmune myasthenia gravis in rats by decreasing effector T cells and altering humoral responses , 2014, Immunology.
[23] P. Oliveira,et al. Doxorubicin‐Induced Cardiotoxicity: From Bioenergetic Failure and Cell Death to Cardiomyopathy , 2014, Medicinal research reviews.
[24] Ying Huang,et al. Circulating Th22 and Th9 Levels in Patients with Acute Coronary Syndrome , 2013, Mediators of inflammation.
[25] D. Chung,et al. IL-9-producing invariant NKT cells protect against DSS-induced colitis in an IL-4-dependent manner , 2012, Mucosal Immunology.
[26] H. Crijns,et al. Doxorubicin-induced cardiomyopathy: from molecular mechanisms to therapeutic strategies. , 2012, Journal of molecular and cellular cardiology.
[27] B. Nourbakhsh,et al. IL‐9 is important for T‐cell activation and differentiation in autoimmune inflammation of the central nervous system , 2011, European journal of immunology.
[28] L. Liaudet,et al. Pharmacological inhibition of CB1 cannabinoid receptor protects against doxorubicin-induced cardiotoxicity. , 2007, Journal of the American College of Cardiology.
[29] M. Okabe,et al. Signal transducer and activator of transcription 3 in the heart transduces not only a hypertrophic signal but a protective signal against doxorubicin-induced cardiomyopathy. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[30] Hong-sheng Zhang,et al. Carvedilol (CAR) combined with carnosic acid (CAA) attenuates doxorubicin-induced cardiotoxicity by suppressing excessive oxidative stress, inflammation, apoptosis and autophagy. , 2019, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.
[31] L-L Pang,et al. IL-9 exacerbates the development of chronic obstructive pulmonary disease through oxidative stress. , 2018, European review for medical and pharmacological sciences.
[32] E. Sanchez,et al. IL-9: Function, Sources, and Detection. , 2017, Methods in molecular biology.
[33] S. Khoury,et al. Th9 cells in the pathogenesis of EAE and multiple sclerosis , 2016, Seminars in Immunopathology.