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symbolscript Corresponding author at:.
被引:19
|作者:
Lin, Siyuan
[1
,2
,3
]
Wang, Qixue
[1
,2
]
Huang, Xiaoting
[1
]
Feng, Jiawei
[1
]
Wang, Yuqing
[1
]
Shao, Tengteng
[1
]
Deng, Xiaofei
[1
]
Cao, Yemin
[1
]
Chen, Xinghua
[4
]
Zhou, Mingmei
[1
,2
]
Zhao, Cheng
[1
]
机构:
[1] Shanghai Univ Tradit Chinese Med, Shanghai Tradit Chinese Med Integrated Hosp, Shanghai 200082, Peoples R China
[2] Shanghai Univ Tradit Chinese Med, Inst Interdisciplinary Med Sci, Shanghai 201203, Peoples R China
[3] Shanghai Univ Tradit Chinese Med, Sch Publ Hlth, Shanghai 201203, Peoples R China
[4] Fudan Univ, Jinshan Hosp, Shanghai, Peoples R China
关键词:
Immune cells;
Inflammation;
Diabetes;
Diabetic wound healing progression;
Cellular components;
Signaling pathways;
STAPHYLOCOCCUS-AUREUS;
GENE-EXPRESSION;
MOUSE MODELS;
WOUND REPAIR;
IN-VIVO;
CELLS;
INFLAMMATION;
RECEPTOR;
MACROPHAGES;
DEACETYLASE;
D O I:
10.1016/j.biopha.2022.114052
中图分类号:
R-3 [医学研究方法];
R3 [基础医学];
学科分类号:
1001 ;
摘要:
A major challenge in the field of diabetic wound healing is to confirm the body's intrinsic mechanism that could sense the immune system damage promptly and protect the wound from non-healing. Accumulating literature indicates that macrophage, a contributor to prolonged inflammation occurring at the wound site, might play such a role in hindering wound healing. Likewise, other immune cell dysfunctions, such as persistent neutrophils and T cell infection, may also lead to persistent oxidative stress and inflammatory reaction during diabetic wound healing. In this article, we discuss recent advances in the immune cellular components in wounds under the diabetic milieu, and the role of key signaling mechanisms that compromise the function of immune cells leading to persistent wound non-healing.
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页数:12
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