Deregulated angiogenesis in chronic lung diseases: a possible role for lung mesenchymal progenitor cells (2017 Grover Conference Series).
Deregulated angiogenesis in chronic lung diseases: a possible role for lung mesenchymal progenitor cells (2017 Grover Conference Series).
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DOI：
10.1177/2045893217739807
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发表时间：
2018-01
影响因子：
2.6
通讯作者：
Majka SM
中科院分区：
文献类型：
--
作者：
Kropski JA;Richmond BW;Gaskill CF;Foronjy RF;Majka SM
慢性肺病（CLD），包括肺纤维化（PF）和慢性阻塞性肺病（COPD），是全球第四大死亡原因。两者都是阻碍整体组织功能的衰弱性病理。CLD的一种常见合并症是血管病，其特征是血管生成失调、重塑和微血管丢失。这大大影响了预后并限制了生存，目前大多数治疗策略主要是姑息性的。血管生成（包括毛细血管和淋巴）与CLD病理生理学的相关性尚未得到解决，因为相互矛盾的证据将血管生成描述为修复性或病理性。因此，我们必须开始理解和模拟肺血管失调的潜在病理学，单独和响应损伤诱导的疾病，以确定维持正常功能和促进修复所必需的细胞相互作用。毛细血管和淋巴管生成在PF和COPD中都是失调的，尽管它们共同调节和构成疾病早期发病机制的机制尚不清楚。调节肺血管稳态、修复和重塑的细胞特异性机制代表了知识上的重大空白，这为开发靶向治疗提供了机会。我们已经表明，ABCG 2阳性多能成体间充质干细胞或祖细胞（MPC）影响毛细血管微血管系统以及淋巴管生成的功能。两者的平衡是正常组织稳态和修复所必需的。我们目前的模型表明，当淋巴和毛细血管生成失衡时，非等效性似乎支持疾病和组织重塑的进展。CLD的血管生成调节机制可能影响其他间质性肺病、结节性硬化症和淋巴管平滑肌瘤病。
Chronic lung disease (CLD), including pulmonary fibrosis (PF) and chronic obstructive pulmonary disease (COPD), is the fourth leading cause of mortality worldwide. Both are debilitating pathologies that impede overall tissue function. A common co-morbidity in CLD is vasculopathy, characterized by deregulated angiogenesis, remodeling, and loss of microvessels. This substantially worsens prognosis and limits survival, with most current therapeutic strategies being largely palliative. The relevance of angiogenesis, both capillary and lymph, to the pathophysiology of CLD has not been resolved as conflicting evidence depicts angiogenesis as both reparative or pathologic. Therefore, we must begin to understand and model the underlying pathobiology of pulmonary vascular deregulation, alone and in response to injury induced disease, to define cell interactions necessary to maintain normal function and promote repair. Capillary and lymphangiogenesis are deregulated in both PF and COPD, although the mechanisms by which they co-regulate and underlie early pathogenesis of disease are unknown. The cell-specific mechanisms that regulate lung vascular homeostasis, repair, and remodeling represent a significant gap in knowledge, which presents an opportunity to develop targeted therapies. We have shown that that ABCG2pos multipotent adult mesenchymal stem or progenitor cells (MPC) influence the function of the capillary microvasculature as well as lymphangiogenesis. A balance of both is required for normal tissue homeostasis and repair. Our current models suggest that when lymph and capillary angiogenesis are out of balance, the non-equivalence appears to support the progression of disease and tissue remodeling. The angiogenic regulatory mechanisms underlying CLD likely impact other interstitial lung diseases, tuberous sclerosis, and lymphangioleiomyomatosis.
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影响因子：
9
作者：
Caramori G;Casolari P;Barczyk A;Durham AL;Di Stefano A;Adcock I
通讯作者：
Adcock I
影响因子：
8.3
作者：
Austin, Eric D;Kawut, Steven M;Abman, Steven H
通讯作者：
Abman, Steven H
影响因子：
7.8
作者：
Banerji, S;Ni, J;Wang, S X;Clasper, S;Su, J;Tammi, R;Jones, M;Jackson, D G
通讯作者：
Jackson, D G
DOI：
10.4049/jimmunol.1500356
发表时间：
2015-09-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
da Silva Antunes R;Madge L;Soroosh P;Tocker J;Croft M
通讯作者：
Croft M
影响因子：
3.7
作者：
An Y;Kiang A;Lopez JP;Kuo SZ;Yu MA;Abhold EL;Chen JS;Wang-Rodriguez J;Ongkeko WM
通讯作者：
Ongkeko WM