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Significance of CXCL12 in Type 2 Diabetes Mellitus and Its Associated Complications.
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- Author(s): Karimabad, Mojgan; Hassanshahi, Gholamhossein
- Source:
Inflammation; Apr2015, Vol. 38 Issue 2, p710-717, 8p- Subject Terms:
- Source:
- Additional Information
- Abstract: Immune responses are extensively accepted as primitive etiological leading causes involved in immune system diseases. It is now well established that chemokines as the main arms of the immune system play critical roles in the regulation of immune responses in the pathogenesis of different diseases. Several environmental and genetic elements of the immune system are also believed to potentially affect both the onsets of immunological diseases. The stromal cell-derived factor-1 alpha (SDF-1α) which in new nomenclature is nominated as C-X-C motif ligand 12 (CXCL12) is involved in the development and progression of immune responses. The CXCL12 is an extensively active chemokine that serves as a recruiter for migration and trafficking of leukocytes and hematopoietic progenitor cells. Patients suffering type 2 diabetes (T2D) that ascribe heterozygous SDF-1 3′A genotype (801G/A in the 3′ untranslated region) have increased insulin-dependent mobilization of adult progenitor cells, which are known to participate in angiogenesis and vascular repair. Conversely, homing of progenitor cells contributes to the diabetes vascular complications. Because carriers of the SDF-1 3′A genotype show increased levels of the CXCL12 messenger RNA (mRNA) in their peripheral blood mononuclear cells. Genetic variations of CXCL12 gene might affect trafficking of inflammatory cells or defected precursors and hence induced tendency to diabetic complications. The SDF-1 3′A genetic variation of CXCL12 influences the development of late vascular diabetic complications, and previous studies reported that this genetic variation regulates the expression of CXCL12. Therefore, the main goal of the present study was to collect the most recent reports regarding the relation between serum concentrations and SDF-1 3′A genetic variation of CXCL12 in T2D. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Inflammation is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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