Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Sep 26;13(9):1338-1348.
doi: 10.4252/wjsc.v13.i9.1338.

Advanced glycation end productions and tendon stem/progenitor cells in pathogenesis of diabetic tendinopathy

Liu Shi  1 , Pan-Pan Lu  1 , Guang-Chun Dai  1 , Ying-Juan Li  2 , Yun-Feng Rui  3
Affiliations
Free PMC article
Review

Advanced glycation end productions and tendon stem/progenitor cells in pathogenesis of diabetic tendinopathy

Liu Shi et al. World J Stem Cells. .
Free PMC article

Abstract

Tendinopathy is a challenging complication observed in patients with diabetes mellitus. Tendinopathy usually leads to chronic pain, limited joint motion, and even ruptured tendons. Imaging and histological analyses have revealed pathological changes in various tendons of patients with diabetes, including disorganized arrangement of collagen fibers, microtears, calcium nodules, and advanced glycation end product (AGE) deposition. Tendon-derived stem/ progenitor cells (TSPCs) were found to maintain hemostasis and to participate in the reversal of tendinopathy. We also discovered the aberrant osteochondrogenesis of TSPCs in vitro. However, the relationship between AGEs and TSPCs in diabetic tendinopathy and the underlying mechanism remain unclear. In this review, we summarize the current findings in this field and hypothesize that AGEs could alter the properties of tendons in patients with diabetes by regulating the proliferation and differentiation of TSPCs in vivo.

Keywords: Advanced glycation end products; Diabetes mellitus; Tendinopathy; Tendon stem/progenitor cells.

PubMed Disclaimer

Conflict of interest statement

Conflict-of-interest statement: The authors have no conflict of interest for this manuscript.

Figures

Figure 1
Figure 1
Hypothesis of the molecular mechanism by which advanced glycation end products regulate the fate of tendon-derived stem/progenitor cells in diabetic tendinopathy. RBCs: Red blood cells; AGEs: Advanced glycation end products; TSPCs: Tendon-derived stem/progenitor cells; RAGE: Receptor for advanced glycation end product; ROS: Reactive oxygen species; TGF-β: Transforming growth factor β.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. de Oliveira RR, Lemos A, de Castro Silveira PV, da Silva RJ, de Moraes SR. Alterations of tendons in patients with diabetes mellitus: a systematic review. Diabet Med. 2011;28:886–895. - PubMed
    1. Shi L, Rui YF, Li G, Wang C. Alterations of tendons in diabetes mellitus: what are the current findings? Int Orthop. 2015;39:1465–1473. - PubMed
    1. Aydeniz A, Gursoy S, Guney E. Which musculoskeletal complications are most frequently seen in type 2 diabetes mellitus? J Int Med Res. 2008;36:505–511. - PubMed
    1. Abate M, Schiavone C, Salini V, Andia I. Management of limited joint mobility in diabetic patients. Diabetes Metab Syndr Obes. 2013;6:197–207. - PMC - PubMed
    1. Lui PPY. Tendinopathy in diabetes mellitus patients-Epidemiology, pathogenesis, and management. Scand J Med Sci Sports. 2017;27:776–787. - PubMed