Literature DB >> 20951732

The impact of redox and thiol status on the bone marrow: Pharmacological intervention strategies.

Christina L Grek1, Danyelle M Townsend, Kenneth D Tew.   

Abstract

Imbalances in cancer cell redox homeostasis provide a platform for new opportunities in the development of anticancer drugs. The control of severe dose-limiting toxicities associated with redox regulation, including myelosuppression and immunosuppression, remains a challenge. Recent evidence implicates a critical role for redox regulation and thiol balance in pathways that control myeloproliferation, hematopoietic progenitor cell mobilization, and immune response. Hematopoietic stem cell (HSC) self-renewal and differentiation are dependent upon levels of intracellular reactive oxygen species (ROS) and niche microenvironments. Redox status and the equilibrium of free thiol:disulfide couples are important in modulating immune response and lymphocyte activation, proliferation and differentiation. This subject matter is the focus of the present review. The potential of redox modulating chemotherapeutics as myeloproliferative and immunomodulatory agents is also covered. Copyright Â
© 2010 Elsevier Inc. All rights reserved.

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Year:  2010        PMID: 20951732      PMCID: PMC3026067          DOI: 10.1016/j.pharmthera.2010.09.008

Source DB:  PubMed          Journal:  Pharmacol Ther        ISSN: 0163-7258            Impact factor:   12.310


  195 in total

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  16 in total

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2.  NADPH oxidase 2 regulates bone marrow microenvironment following hindlimb ischemia: role in reparative mobilization of progenitor cells.

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3.  Processing of CXCL12 by different osteoblast-secreted cathepsins.

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Review 5.  Oxidases and reactive oxygen species during hematopoiesis: a focus on megakaryocytes.

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7.  In vivo response to dynamic hyaluronic acid hydrogels.

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Review 8.  Novel roles of reactive oxygen species in the pathogenesis of acute myeloid leukemia.

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9.  S-Glutathionylation of estrogen receptor α affects dendritic cell function.

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Review 10.  Causes and consequences of cysteine S-glutathionylation.

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