Jiaqian Huang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Jiaqian Huang has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Huiying Liu
School of Stomatology, Dalian Medical University , Dalian 116044
1 shared publication - Siyu Zhu
Department of Oral Pathology, School of Dentistry, Chonnam National University, Gwangju 61186, Republic of Korea
1 shared publication - Wenqi Fu
School of Stomatology, Dalian Medical University, No. 9 West Section, Lvshun South Road, Dalian 116044, China
1 shared publication - Yaran Zang
School of Stomatology, Dalian Medical University, No. 9 West Section, Lvshun South Road, Dalian 116044, China
1 shared publication - Yunmeng Tong
School of Stomatology, Dalian Medical University, No. 9 West Section, Lvshun South Road, Dalian 116044, China
1 shared publication - Yuzhu He
School of Stomatology, Dalian Medical University, Dalian 116044, China
1 shared publication
Latest Publications
- Open Access
- 12 June 2025
- Published by MDPI AG in Biomedicines
- Vol. 13 (6) , 1454
The Mechanism of Simvastatin-Mediated M1 Macrophage Polarization Contributing to Osteogenesis and Angiogenesis
Background: The immune response is essential for bone regeneration, and macrophages in the immune microenvironment contribute to bone metabolism and angiogenesis. Emerging evidence demonstrates that simvastatin is a promising candidate for bone repair and promotes bone formation both in vitro and in vivo. However, the effect of simvastatin on macrophages and the following outcomes are still unclear. Objectives: This study aimed to investigate the potential immunomodulatory effect of simvastatin on M1 macrophages and its subsequent impact on osteogenesis and angiogenesis. Methods: Cell viability was assessed by CCK-8. Osteogenic and angiogenic markers were evaluated by RT-qPCR, Western blotting, and immunofluorescence. M1 macrophage phenotype was analyzed by flow cytometry. Osteogenesis was examined by histological staining, and angiogenic capacity was assessed using functional assays. Results: The present study found that simvastatin decreased M1 macrophage markers (CD86) and stimulated M1 macrophages to express high levels of pro-regenerative cytokines (BMP-2 and VEGF). In addition, simvastatin promoted osteogenic differentiation in MC3T3-E1 cells and angiogenic gene expression in HUVECs. Importantly, simvastatin enhanced the osteogenic capacity of MC3T3-E1 and the angiogenic potential of HUVECs by inhibiting M1 macrophage polarization in vitro. Conclusions: We demonstrated that simvastatin could confer favorable bone immunomodulatory properties and influence the crosstalk behavior between immune cells and osteoblasts and vascular endothelial cells to promote bone healing.
- 12 June 2025
- Published by MDPI AG in Biomedicines
- Vol. 13 (6) , 1454
Open AccessThe Mechanism of Simvastatin-Mediated M1 Macrophage Polarization Contributing to Osteogenesis and Angiogenesis
Background: The immune response is essential for bone regeneration, and macrophages in the immune microenvironment contribute to bone metabolism and angiogenesis. Emerging evidence demonstrates that simvastatin is a promising candidate for bone repair and promotes bone formation both in vitro and in vivo. However, the effect of simvastatin on macrophages and the following outcomes are still unclear. Objectives: This study aimed to investigate the potential immunomodulatory effect of simvastatin on M1 macrophages and its subsequent impact on osteogenesis and angiogenesis. Methods: Cell viability was assessed by CCK-8. Osteogenic and angiogenic markers were evaluated by RT-qPCR, Western blotting, and immunofluorescence. M1 macrophage phenotype was analyzed by flow cytometry. Osteogenesis was examined by histological staining, and angiogenic capacity was assessed using functional assays. Results: The present study found that simvastatin decreased M1 macrophage markers (CD86) and stimulated M1 macrophages to express high levels of pro-regenerative cytokines (BMP-2 and VEGF). In addition, simvastatin promoted osteogenic differentiation in MC3T3-E1 cells and angiogenic gene expression in HUVECs. Importantly, simvastatin enhanced the osteogenic capacity of MC3T3-E1 and the angiogenic potential of HUVECs by inhibiting M1 macrophage polarization in vitro. Conclusions: We demonstrated that simvastatin could confer favorable bone immunomodulatory properties and influence the crosstalk behavior between immune cells and osteoblasts and vascular endothelial cells to promote bone healing.