Open AccessPioglitazone attenuates advanced glycation end products‐induced apoptosis and calcification by modulating autophagy in tendon‐derived stem cells
Author(s) -
Xu Langhai,
Xu Kai,
Wu Zhipeng,
Chen Zhonggai,
He Yuzhe,
Ma Chiyuan,
Moqbel Safwat A. A.,
Ran Jisheng,
Zhang Caihua,
Wu Lidong,
Xiong Yan
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14901
Subject(s) - autophagy , glycation , pioglitazone , tendinopathy , advanced glycation end product , calcification , apoptosis , medicine , diabetes mellitus , endocrinology , annexin , cancer research , tendon , pathology , chemistry , type 2 diabetes , biochemistry
Diabetes mellitus (DM) is one of the prominent risk factors for pathological development and progression of tendinopathy. One feature of DM‐related changes in tendinopathy is accumulation of advanced glycation end products (AGEs) in affected tendons. Pioglitazone (Pio), a peroxisome proliferator‐activated receptor γ agonist, performs a protective effect against AGEs. The present study aimed to investigate the pathogenetic role of AGEs on tendon‐derived stem cells (TDSCs) and to determine the effect of Pio on AGEs‐induced TDSC dysfunctions. Results indicated that AGEs induced TDSC apoptosis as well as compensatory activation of autophagy. Pharmacologic activation/inhibition of autophagy leaded to alleviate/exacerbate apoptosis induced by AGEs. We further confirmed the effect of Pio on autophagy, which ameliorated apoptosis and abnormal calcification caused by AGEs both in vitro and in vivo. Thus, we suggest that Pio ameliorates the dysfunctions of TDSCs against AGEs by promoting autophagy, and we also reveal that Pio is a potential pharmacological choice for tendinopathy.