Fenofibrate increases cardiac autophagy via FGF21/SIRT1 and prevents fibrosis and inflammation in the hearts of Type 1 diabetic mice

2016 ◽  
Vol 130 (8) ◽  
pp. 625-641 ◽  
Author(s):  
Jingjing Zhang ◽  
Yanli Cheng ◽  
Junlian Gu ◽  
Shudong Wang ◽  
Shanshan Zhou ◽  
...  

Fenofibrate (FF) as a commonly-used lipid-lowering medicine in clinics was examined for its potentially repurposing to prevent the cardiac abnormalities in patients with type 1 diabetes. We demonstrated here that fenofibrate significantly prevented diabetes-induced cardiac dysfunction and remodeling in fibroblast growth factor 21 (FGF21)-dependent manner.

Diabetes ◽  
2018 ◽  
Vol 67 (5) ◽  
pp. 974-985 ◽  
Author(s):  
Zhongjie Fu ◽  
Zhongxiao Wang ◽  
Chi-Hsiu Liu ◽  
Yan Gong ◽  
Bertan Cakir ◽  
...  

Blood ◽  
1992 ◽  
Vol 80 (8) ◽  
pp. 1905-1913 ◽  
Author(s):  
A Bikfalvi ◽  
ZC Han ◽  
G Fuhrmann

Abstract We have investigated the interaction of fibroblast growth factor (FGF) with megakaryocytopoiesis. Acidic FGF (aFGF) stimulated the proliferation of murine megakaryocytes and human erythroleukemia (HEL) cells in a concentration-dependent manner. The concentrations of aFGF required to elicit half-maximum and maximum effects were similar for HEL and megakaryocytic colony formation. The effect of aFGF was comparable to that of basic FGF (bFGF) in both cell types. The effect of both FGFs was found to be synergistic with interleukin-3 (IL-3), and was abrogated by a monoclonal anti-IL-6 antibody. A specific cell surface receptor complex of approximately 120 Kd was detected for FGF by crosslinking experiments on HEL cells and total bone marrow (BM) cells. Single-cell autoradiography of megakaryocytes in BM smears and BM cultures showed binding sites for 125I-aFGF. Northern blot analysis of messenger RNA (mRNA) from total BM and HEL cells showed a 4.4-kb mRNA specific for FGF receptors type 1 (flg) and type 2 (bek). This was confirmed by polymerase chain reaction, which also showed the presence of FGF receptor mRNA in megakaryocytic-like cells, normal megakaryocytes, and platelets. Together, these results indicate that FGF is involved in megakaryocytopoiesis and suggest that this interaction may be mediated via FGF receptor type 1 and type 2 located on the megakaryocytic lineage or on accessory cells responsible for the release of megakaryocytic growth-promoting activities.


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