首页/数据集/Macrophage-specific alfa5 integrin signaling protects the infarcted heart from adverse remodeling, by stimulating angiogenesis. Macrophage-specific alfa5 integrin signaling protects the infarcted heart from adverse remodeling, by stimulating angiogenesis

Macrophage-specific alfa5 integrin signaling protects the infarcted heart from adverse remodeling, by stimulating angiogenesis. Macrophage-specific alfa5 integrin signaling protects the infarcted heart from adverse remodeling, by stimulating angiogenesis

NIAID Data Ecosystem2026-03-13 收录

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巨噬细胞血管生成

数据链接：

https://www.ncbi.nlm.nih.gov/bioproject/PRJNA788538 数据链接链接失效反馈

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资源简介：

This SuperSeries is composed of the SubSeries listed below. Overall design: Refer to individual Series

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创建时间：

2021-12-13

心肌梗死巨噬细胞表观遗传

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Our study comprehensively investigated the epigenetic features of cardiac F4/80+CD45+ macrophages at 3 and 7 days after P1 and P10 MI at infarct, border, and remote zones of mouse hearts (IZ, BZ, and

NIAID Data Ecosystem30

Bone Marrow SSEA1+ Cells Support the Myocardium in Cardiac Pressure Overload

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干细胞治疗

RationaleStage specific embryonic antigen 1+ (SSEA1+) cells have been described as the most primitive mesenchymal progenitor cell in the bone marrow. Cardiac injury mobilizes SSEA1+ cells into the per

Figshare2016-01-18 更新20

Bone marrow macrophage derived GPNMB protein binds to orphan receptor GPR39 and plays a critical role in cardiac repair. Bone marrow macrophage derived GPNMB protein binds to orphan receptor GPR39 and plays a critical role in cardiac repair

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GPNMB-GPR39信号通路

Levels of Glyco Protein Non-metastatic Melanoma protein B (GPNMB), a type I transmembrane protein, originally identified in non-metastatic melanomas has been shown to be strongly associated with human

NIAID Data Ecosystem10

YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction. YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction

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巨噬细胞极化

Adverse cardiac remodeling after myocardial infarction (MI) causes structural and functional changes in the heart leading to heart failure. The initial pro-inflammatory response followed by an anti-in

NIAID Data Ecosystem30

The human kidney capsule contains a functionally distinct mesenchymal stromal cell population

间充质基质细胞

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We recently demonstrated that the adult human kidney cortex contains a perivascular stromal cell (kPSC) that shows organotypic properties and is important for repair and stabilisation of kidney functi

Figshare2017-12-06 更新20

Macrophage-specific alfa5 integrin signaling protects the infarcted heart from adverse remodeling, by stimulating angiogenesis. Macrophage-specific alfa5 integrin signaling protects the infarcted heart from adverse remodeling, by stimulating angiogenesis

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