Spandidos Publications Logo
  • About
    • About Spandidos
    • Aims and Scopes
    • Abstracting and Indexing
    • Editorial Policies
    • Reprints and Permissions
    • Job Opportunities
    • Terms and Conditions
    • Contact
  • Journals
    • All Journals
    • Oncology Letters
      • Oncology Letters
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • International Journal of Oncology
      • International Journal of Oncology
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Molecular and Clinical Oncology
      • Molecular and Clinical Oncology
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Experimental and Therapeutic Medicine
      • Experimental and Therapeutic Medicine
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • International Journal of Molecular Medicine
      • International Journal of Molecular Medicine
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Biomedical Reports
      • Biomedical Reports
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Oncology Reports
      • Oncology Reports
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Molecular Medicine Reports
      • Molecular Medicine Reports
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • World Academy of Sciences Journal
      • World Academy of Sciences Journal
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • International Journal of Functional Nutrition
      • International Journal of Functional Nutrition
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • International Journal of Epigenetics
      • International Journal of Epigenetics
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Medicine International
      • Medicine International
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
  • Articles
  • Information
    • Information for Authors
    • Information for Reviewers
    • Information for Librarians
    • Information for Advertisers
    • Conferences
  • Language Editing
Spandidos Publications Logo
  • About
    • About Spandidos
    • Aims and Scopes
    • Abstracting and Indexing
    • Editorial Policies
    • Reprints and Permissions
    • Job Opportunities
    • Terms and Conditions
    • Contact
  • Journals
    • All Journals
    • Biomedical Reports
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Experimental and Therapeutic Medicine
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • International Journal of Epigenetics
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • International Journal of Functional Nutrition
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • International Journal of Molecular Medicine
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • International Journal of Oncology
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Medicine International
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Molecular and Clinical Oncology
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Molecular Medicine Reports
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Oncology Letters
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • Oncology Reports
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
    • World Academy of Sciences Journal
      • Information for Authors
      • Editorial Policies
      • Editorial Board
      • Aims and Scope
      • Abstracting and Indexing
      • Bibliographic Information
      • Archive
  • Articles
  • Information
    • For Authors
    • For Reviewers
    • For Librarians
    • For Advertisers
    • Conferences
  • Language Editing
Login Register Submit
  • This site uses cookies
  • You can change your cookie settings at any time by following the instructions in our Cookie Policy. To find out more, you may read our Privacy Policy.

    I agree
Search articles by DOI, keyword, author or affiliation
Search
Advanced Search
presentation
International Journal of Molecular Medicine
Join Editorial Board Propose a Special Issue
Print ISSN: 1107-3756 Online ISSN: 1791-244X
Journal Cover
July-2017 Volume 40 Issue 1

Full Size Image

Sign up for eToc alerts
Recommend to Library

Journals

International Journal of Molecular Medicine

International Journal of Molecular Medicine

International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

International Journal of Oncology

International Journal of Oncology

International Journal of Oncology is an international journal devoted to oncology research and cancer treatment.

Molecular Medicine Reports

Molecular Medicine Reports

Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.

Oncology Reports

Oncology Reports

Oncology Reports is an international journal devoted to fundamental and applied research in Oncology.

Experimental and Therapeutic Medicine

Experimental and Therapeutic Medicine

Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine.

Oncology Letters

Oncology Letters

Oncology Letters is an international journal devoted to Experimental and Clinical Oncology.

Biomedical Reports

Biomedical Reports

Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology.

Molecular and Clinical Oncology

Molecular and Clinical Oncology

International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis.

World Academy of Sciences Journal

World Academy of Sciences Journal

Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology.

International Journal of Functional Nutrition

International Journal of Functional Nutrition

Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition.

International Journal of Epigenetics

International Journal of Epigenetics

Publishes open-access research on using epigenetics to advance understanding and treatment of human disease.

Medicine International

Medicine International

An International Open Access Journal Devoted to General Medicine.

Journal Cover
July-2017 Volume 40 Issue 1

Full Size Image

Sign up for eToc alerts
Recommend to Library

  • Article
  • Citations
    • Cite This Article
    • Download Citation
    • Create Citation Alert
    • Remove Citation Alert
    • Cited By
  • Similar Articles
    • Related Articles (in Spandidos Publications)
    • Similar Articles (Google Scholar)
    • Similar Articles (PubMed)
  • Download PDF
  • Download XML
  • View XML
Article

A novel damage mechanism: Contribution of the interaction between necroptosis and ROS to high glucose-induced injury and inflammation in H9c2 cardiac cells

  • Authors:
    • Weijie Liang
    • Meiji Chen
    • Dongdan Zheng
    • Jieyi He
    • Mingcai Song
    • Liqiu Mo
    • Jianqiang Feng
    • Jun Lan
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, Central Hospital of Panyu District, Guangzhou, Guangdong 511400, P.R. China, Department of Pediatrics, Huangpu Division of The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510700, P.R. China, Department of Cardiac Care Unit, Huangpu Division of The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510700, P.R. China, Department of Anesthesiology, Huangpu Division of The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510700, P.R. China, Department of Cardiology, The Third People's Hospital of Dongguan, Dongguan, Guangdong 523326, P.R. China
  • Pages: 201-208
    |
    Published online on: May 29, 2017
       https://doi.org/10.3892/ijmm.2017.3006
  • Expand metrics +
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Cited By (CrossRef): 0 citations Loading Articles...

This article is mentioned in:



Abstract

Recently, a novel mechanism known as ‘programmed necrosis’ or necroptosis has been shown to be another important mechanism of cell death in the heart. In this study, we investigated the role of necroptosis in high glucose (HG)-induced injury and inflammation, as well as the underlying mechanisms. In particular, we focused on the interaction between necroptosis and reactive oxygen species (ROS) in H9c2 cardiac cells. Our results demonstrated that the exposure of H9c2 cardiac cells to 35 mM glucose (HG) markedly enhanced the expression level of receptor-interacting protein 3 (RIP3), a kinase which promotes necroptosis. Importantly, co-treatment of the cells with 100 µM necrostatin-1 (a specific inhibitor of necroptosis) and HG for 24 h attenuated not only the increased expression level of RIP3, but also the HG-induced injury and inflammation, as evidenced by an increase in cell viability, a decrease in ROS generation, the attenuation of the dissipation of mitochondrial membrane potential and a decrese in the secretion levels of inflammatory cytokines, i.e., interleukin (IL)-1β and tumor necrosis factor (TNF)-α. Furthermore, treatment of the cells with 1 mM N-acetyl‑L‑cysteine (a scavenger of ROS) for 60 min prior to exposure to HG significantly reduced the HG-induced increase in the RIP3 expression level, as well as the injury and inflammatory response described above. Taken together, the findings of this study clearly demonstrate a novel damage mechanism involving the positive interaction between necroptosis and ROS attributing to HG-induced injury and inflammation in H9c2 cardiac cells.
View Figures

Figure 1

Figure 2

Figure 3

Figure 4

Figure 5

Figure 6

View References

1 

Brownlee M: Biochemistry and molecular cell biology of diabetic complications. Nature. 414:813–820. 2001. View Article : Google Scholar : PubMed/NCBI

2 

Ren J and Davidoff AJ: Diabetes rapidly induces contractile dysfunctions in isolated ventricular myocytes. Am J Physiol. 272:H148–H158. 1997.PubMed/NCBI

3 

Xu W, Wu W, Chen J, Guo R, Lin J, Liao X and Feng J: Exogenous hydrogen sulfide protects H9c2 cardiac cells against high glucose-induced injury by inhibiting the activities of the p38 MAPK and ERK1/2 pathways. Int J Mol Med. 32:917–925. 2013.PubMed/NCBI

4 

Soetikno V, Sari FR, Sukumaran V, Lakshmanan AP, Mito S, Harima M, Thandavarayan RA, Suzuki K, Nagata M, Takagi R, et al: Curcumin prevents diabetic cardiomyopathy in streptozotocin-induced diabetic rats: possible involvement of PKC-MAPK signaling pathway. Eur J Pharm Sci. 47:604–614. 2012. View Article : Google Scholar : PubMed/NCBI

5 

Peake BF, Nicholson CK, Lambert JP, Hood RL, Amin H, Amin S and Calvert JW: Hydrogen sulfide preconditions the db/db diabetic mouse heart against ischemia-reperfusion injury by activating Nrf2 signaling in an Erk-dependent manner. Am J Physiol Heart Circ Physiol. 304:H1215–H1224. 2013. View Article : Google Scholar : PubMed/NCBI

6 

Chen J, Mo H, Guo R, You Q, Huang R and Wu K: Inhibition of the leptin-induced activation of the p38 MAPK pathway contributes to the protective effects of naringin against high glucose-induced injury in H9c2 cardiac cells. Int J Mol Med. 33:605–612. 2014.PubMed/NCBI

7 

Huang H and Wu K, You Q, Huang R, Li S and Wu K: Naringin inhibits high glucose-induced cardiomyocyte apoptosis by attenuating mitochondrial dysfunction and modulating the activation of the p38 signaling pathway. Int J Mol Med. 32:396–402. 2013.PubMed/NCBI

8 

Cai L, Li W, Wang G, Guo L, Jiang Y and Kang YJ: Hyperglycemia-induced apoptosis in mouse myocardium: mitochondrial cytochrome C-mediated caspase-3 activation pathway. Diabetes. 51:1938–1948. 2002. View Article : Google Scholar : PubMed/NCBI

9 

Chen J, Guo R, Yan H, Tian L, You Q, Li S, Huang R and Wu K: Naringin inhibits ROS-activated MAPK pathway in high glucose-induced injuries in H9c2 cardiac cells. Basic Clin Pharmacol Toxicol. 114:293–304. 2014. View Article : Google Scholar

10 

Fiordaliso F, Leri A, Cesselli D, Limana F, Safai B, Nadal-Ginard B, Anversa P and Kajstura J: Hyperglycemia activates p53 and p53-regulated genes leading to myocyte cell death. Diabetes. 50:2363–2375. 2001. View Article : Google Scholar : PubMed/NCBI

11 

Fei L, Yong-Jun H, Zhang-Min M, Bing X, Shuang W, Qian-qian S and Jun L: Rosiglitazone attenuates memory impairment in aged rat with diabetes by inhibiting NF-kappa B signal pathway activation. Exp Clin Endocrinol Diabetes. 123:536–542. 2015. View Article : Google Scholar : PubMed/NCBI

12 

Thandavarayan RA, Giridharan VV, Sari FR, Arumugam S, Veeraveedu PT, Pandian GN, Palaniyandi SS, Ma M, Suzuki K, Gurusamy N, et al: Depletion of 14-3-3 protein exacerbates cardiac oxidative stress, inflammation and remodeling process via modulation of MAPK/NF-κB signaling pathways after streptozotocin-induced diabetes mellitus. Cell Physiol Biochem. 28:911–922. 2011. View Article : Google Scholar

13 

Xu W, Chen J, Lin J, Liu D, Mo L, Pan W, Feng J, Wu W and Zheng D: Exogenous H S protects H9c2 cardiac cells against high glucose-induced injury 2 and inflammation by inhibiting the activation of the NF-κB and IL-1β pathways. Int J Mol Med. 35:177–186. 2015.

14 

Kung G, Konstantinidis K and Kitsis RN: Programmed necrosis, not apoptosis, in the heart. Circ Res. 108:1017–1036. 2011. View Article : Google Scholar : PubMed/NCBI

15 

Declercq W, Vanden Berghe T and Vandenabeele P: RIP kinases at the crossroads of cell death and survival. Cell. 138:229–232. 2009. View Article : Google Scholar : PubMed/NCBI

16 

Zhang DW, Shao J, Lin J, Zhang N, Lu BJ, Lin SC, Dong MQ and Han J: RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis. Science. 325:332–336. 2009. View Article : Google Scholar : PubMed/NCBI

17 

He S, Wang L, Miao L, Wang T, Du F, Zhao L and Wang X: Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. Cell. 137:1100–1111. 2009. View Article : Google Scholar : PubMed/NCBI

18 

Cho YS, Challa S, Moquin D, Genga R, Ray TD, Guildford M and Chan FK: Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation. Cell. 137:1112–1123. 2009. View Article : Google Scholar : PubMed/NCBI

19 

Linkermann A, Hackl MJ, Kunzendorf U, Walczak H, Krautwald S and Jevnikar AM: Necroptosis in immunity and ischemia-reperfusion injury. Am J Transplant. 13:2797–2804. 2013. View Article : Google Scholar : PubMed/NCBI

20 

Dmitriev YV, Minasian SM, Demchenko EA and Galagudza MM: Study of cardioprotective effects of necroptosis inhibitors on isolated rat heart subjected to global ischemia-reperfusion. Bull Exp Biol Med. 155:245–248. 2013. View Article : Google Scholar : PubMed/NCBI

21 

Koshinuma S, Miyamae M, Kaneda K, Kotani J and Figueredo VM: Combination of necroptosis and apoptosis inhibition enhances cardioprotection against myocardial ischemia-reperfusion injury. J Anesth. 28:235–241. 2014. View Article : Google Scholar

22 

Liu YS, Huang ZW, Wang L, Liu XX, Wang YM, Zhang Y and Zhang M: Sitagliptin alleviated myocardial remodeling of the left ventricle and improved cardiac diastolic dysfunction in diabetic rats. J Pharmacol Sci. 127:260–274. 2015. View Article : Google Scholar : PubMed/NCBI

23 

Oerlemans MI, Liu J, Arslan F, den Ouden K, van Middelaar BJ, Doevendans PA and Sluijter JP: Inhibition of RIP1-dependent necrosis prevents adverse cardiac remodeling after myocardial ischemia-reperfusion in vivo. Basic Res Cardiol. 107:2702012. View Article : Google Scholar : PubMed/NCBI

24 

Lim SY, Davidson SM, Mocanu MM, Yellon DM and Smith CC: The cardioprotective effect of necrostatin requires the cyclophilin-D component of the mitochondrial permeability transition pore. Cardiovasc Drugs Ther. 21:467–469. 2007. View Article : Google Scholar : PubMed/NCBI

25 

Smith CC, Davidson SM, Lim SY, Simpkin JC, Hothersall JS and Yellon DM: Necrostatin: a potentially novel cardioprotective agent? Cardiovasc Drugs Ther. 21:227–233. 2007. View Article : Google Scholar : PubMed/NCBI

26 

Luedde M, Lutz M, Carter N, Sosna J, Jacoby C, Vucur M, Gautheron J, Roderburg C, Borg N, Reisinger F, et al: RIP3, a kinase promoting necroptotic cell death, mediates adverse remodelling after myocardial infarction. Cardiovasc Res. 103:206–216. 2014. View Article : Google Scholar : PubMed/NCBI

27 

Meng L, Jin W and Wang X: RIP3-mediated necrotic cell death accelerates systematic inflammation and mortality. Proc Natl Acad Sci USA. 112:11007–11012. 2015. View Article : Google Scholar : PubMed/NCBI

28 

Han D, Ybanez MD, Ahmadi S, Yeh K and Kaplowitz N: Redox regulation of tumor necrosis factor signaling. Antioxid Redox Signal. 11:2245–2263. 2009. View Article : Google Scholar : PubMed/NCBI

29 

Morgan MJ and Liu ZG: Reactive oxygen species in TNFalpha-induced signaling and cell death. Mol Cells. 30:1–12. 2010. View Article : Google Scholar : PubMed/NCBI

30 

Fortes GB, Alves LS, de Oliveira R, Dutra FF, Rodrigues D, Fernandez PL, Souto-Padron T, De Rosa MJ, Kelliher M, Golenbock D, et al: Heme induces programmed necrosis on macrophages through autocrine TNF and ROS production. Blood. 119:2368–2375. 2012. View Article : Google Scholar : PubMed/NCBI

31 

Ye YC, Wang HJ, Yu L, Tashiro S, Onodera S and Ikejima T: RIP1-mediated mitochondrial dysfunction and ROS production contributed to tumor necrosis factor alpha-induced L929 cell necroptosis and autophagy. Int Immunopharmacol. 14:674–682. 2012. View Article : Google Scholar : PubMed/NCBI

32 

Yu X, Deng Q, Li W, Xiao L, Luo X, Liu X, Yang L, Peng S, Ding Z, Feng T, et al: Neoalbaconol induces cell death through necroptosis by regulating RIPK-dependent autocrine TNFα and ROS production. Oncotarget. 6:1995–2008. 2015. View Article : Google Scholar : PubMed/NCBI

33 

Kikuchi M, Kuroki S, Kayama M, Sakaguchi S, Lee KK and Yonehara S: Protease activity of procaspase-8 is essential for cell survival by inhibiting both apoptotic and nonapoptotic cell death dependent on receptor-interacting protein kinase 1 (RIP1) and RIP3. J Biol Chem. 287:41165–41173. 2012. View Article : Google Scholar : PubMed/NCBI

34 

Schenk B and Fulda S: Reactive oxygen species regulate Smac mimetic/TNFα-induced necroptotic signaling and cell death. Oncogene. 34:5796–5806. 2015. View Article : Google Scholar : PubMed/NCBI

35 

Nunes T, Bernardazzi C and de Souza HS: Cell death and inflammatory bowel diseases: apoptosis, necrosis, and autophagy in the intestinal epithelium. BioMed Res Int. 2014:2184932014. View Article : Google Scholar : PubMed/NCBI

36 

Fenton K: The effect of cell death in the initiation of lupus nephritis. Clin Exp Immunol. 179:11–16. 2015. View Article : Google Scholar

37 

Su Z, Yang Z, Xu Y, Chen Y and Yu Q: Apoptosis, autophagy, necroptosis, and cancer metastasis. Mol Cancer. 14:482015. View Article : Google Scholar : PubMed/NCBI

38 

Fang ZY, Prins JB and Marwick TH: Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications. Endocr Rev. 25:543–567. 2004. View Article : Google Scholar : PubMed/NCBI

39 

Shimomura H, Terasaki F, Hayashi T, Kitaura Y, Isomura T and Suma H: Autophagic degeneration as a possible mechanism of myocardial cell death in dilated cardiomyopathy. Jpn Circ J. 65:965–968. 2001. View Article : Google Scholar : PubMed/NCBI

40 

Vanlangenakker N, Vanden Berghe T and Vandenabeele P: Many stimuli pull the necrotic trigger, an overview. Cell Death Differ. 19:75–86. 2012. View Article : Google Scholar :

41 

Boudina S, Sena S, Theobald H, Sheng X, Wright JJ, Hu XX, Aziz S, Johnson JI, Bugger H, Zaha VG, et al: Mitochondrial energetics in the heart in obesity-related diabetes: direct evidence for increased uncoupled respiration and activation of uncoupling proteins. Diabetes. 56:2457–2466. 2007. View Article : Google Scholar : PubMed/NCBI

42 

Agrawal NK and Kant S: Targeting inflammation in diabetes: newer therapeutic options. World J Diabetes. 5:697–710. 2014. View Article : Google Scholar : PubMed/NCBI

43 

Fang Q, Wang J, Wang L, Zhang Y, Yin H, Li Y, Tong C, Liang G and Zheng C: Attenuation of inflammatory response by a novel chalcone protects kidney and heart from hyperglycemia-induced injuries in type 1 diabetic mice. Toxicol Appl Pharmacol. 288:179–191. 2015. View Article : Google Scholar : PubMed/NCBI

44 

Yu X, Deng Q, Bode AM, Dong Z and Cao Y: The role of necroptosis, an alternative form of cell death, in cancer therapy. Expert Rev Anticancer Ther. 13:883–893. 2013. View Article : Google Scholar : PubMed/NCBI

45 

Yang Y, Jiang G, Zhang P and Fan J: Programmed cell death and its role in inflammation. Mil Med Res. 2:122015. View Article : Google Scholar : PubMed/NCBI

46 

Liu ZY, Wu B, Guo YS, Zhou YH, Fu ZG, Xu BQ, Li JH, Jing L, Jiang JL, Tang J, et al: Necrostatin-1 reduces intestinal inflammation and colitis-associated tumorigenesis in mice. Am J Cancer Res. 5:3174–3185. 2015.PubMed/NCBI

Related Articles

  • Abstract
  • View
  • Download
  • Twitter
Copy and paste a formatted citation
Spandidos Publications style
Liang W, Chen M, Zheng D, He J, Song M, Mo L, Feng J and Lan J: A novel damage mechanism: Contribution of the interaction between necroptosis and ROS to high glucose-induced injury and inflammation in H9c2 cardiac cells. Int J Mol Med 40: 201-208, 2017.
APA
Liang, W., Chen, M., Zheng, D., He, J., Song, M., Mo, L. ... Lan, J. (2017). A novel damage mechanism: Contribution of the interaction between necroptosis and ROS to high glucose-induced injury and inflammation in H9c2 cardiac cells. International Journal of Molecular Medicine, 40, 201-208. https://doi.org/10.3892/ijmm.2017.3006
MLA
Liang, W., Chen, M., Zheng, D., He, J., Song, M., Mo, L., Feng, J., Lan, J."A novel damage mechanism: Contribution of the interaction between necroptosis and ROS to high glucose-induced injury and inflammation in H9c2 cardiac cells". International Journal of Molecular Medicine 40.1 (2017): 201-208.
Chicago
Liang, W., Chen, M., Zheng, D., He, J., Song, M., Mo, L., Feng, J., Lan, J."A novel damage mechanism: Contribution of the interaction between necroptosis and ROS to high glucose-induced injury and inflammation in H9c2 cardiac cells". International Journal of Molecular Medicine 40, no. 1 (2017): 201-208. https://doi.org/10.3892/ijmm.2017.3006
Copy and paste a formatted citation
x
Spandidos Publications style
Liang W, Chen M, Zheng D, He J, Song M, Mo L, Feng J and Lan J: A novel damage mechanism: Contribution of the interaction between necroptosis and ROS to high glucose-induced injury and inflammation in H9c2 cardiac cells. Int J Mol Med 40: 201-208, 2017.
APA
Liang, W., Chen, M., Zheng, D., He, J., Song, M., Mo, L. ... Lan, J. (2017). A novel damage mechanism: Contribution of the interaction between necroptosis and ROS to high glucose-induced injury and inflammation in H9c2 cardiac cells. International Journal of Molecular Medicine, 40, 201-208. https://doi.org/10.3892/ijmm.2017.3006
MLA
Liang, W., Chen, M., Zheng, D., He, J., Song, M., Mo, L., Feng, J., Lan, J."A novel damage mechanism: Contribution of the interaction between necroptosis and ROS to high glucose-induced injury and inflammation in H9c2 cardiac cells". International Journal of Molecular Medicine 40.1 (2017): 201-208.
Chicago
Liang, W., Chen, M., Zheng, D., He, J., Song, M., Mo, L., Feng, J., Lan, J."A novel damage mechanism: Contribution of the interaction between necroptosis and ROS to high glucose-induced injury and inflammation in H9c2 cardiac cells". International Journal of Molecular Medicine 40, no. 1 (2017): 201-208. https://doi.org/10.3892/ijmm.2017.3006
Follow us
  • Twitter
  • LinkedIn
  • Facebook
About
  • Spandidos Publications
  • Careers
  • Cookie Policy
  • Privacy Policy
How can we help?
  • Help
  • Live Chat
  • Contact
  • Email to our Support Team