Therapeutic Potential of Endothelial Colony-Forming Cells in Ischemic Disease: Strategies to Improve their Regenerative Efficacy.
Therapeutic Potential of Endothelial Colony-Forming Cells in Ischemic Disease: Strategies to Improve their Regenerative Efficacy.
复制标题
DOI:
10.3390/ijms21197406
复制
发表时间:
2020-10-07
影响因子:
5.6
通讯作者:
Moccia F
中科院分区:
文献类型:
--
作者:
Faris P;Negri S;Perna A;Rosti V;Guerra G;Moccia F
Cardiovascular disease (CVD) comprises a range of major clinical cardiac and circulatory diseases, which produce immense health and economic burdens worldwide. Currently, vascular regenerative surgery represents the most employed therapeutic option to treat ischemic disorders, even though not all the patients are amenable to surgical revascularization. Therefore, more efficient therapeutic approaches are urgently required to promote neovascularization. Therapeutic angiogenesis represents an emerging strategy that aims at reconstructing the damaged vascular network by stimulating local angiogenesis and/or promoting de novo blood vessel formation according to a process known as vasculogenesis. In turn, circulating endothelial colony-forming cells (ECFCs) represent truly endothelial precursors, which display high clonogenic potential and have the documented ability to originate de novo blood vessels in vivo. Therefore, ECFCs are regarded as the most promising cellular candidate to promote therapeutic angiogenesis in patients suffering from CVD. The current briefly summarizes the available information about the origin and characterization of ECFCs and then widely illustrates the preclinical studies that assessed their regenerative efficacy in a variety of ischemic disorders, including acute myocardial infarction, peripheral artery disease, ischemic brain disease, and retinopathy. Then, we describe the most common pharmacological, genetic, and epigenetic strategies employed to enhance the vasoreparative potential of autologous ECFCs by manipulating crucial pro-angiogenic signaling pathways, e.g., extracellular-signal regulated kinase/Akt, phosphoinositide 3-kinase, and Ca2+ signaling. We conclude by discussing the possibility of targeting circulating ECFCs to rescue their dysfunctional phenotype and promote neovascularization in the presence of CVD.
登录
查看更多内容
影响因子:
56.9
作者:
Asahara, T;Murohara, T;Isner, JM
通讯作者:
Isner, JM
影响因子:
5.4
作者:
Bouvard C;Galy-Fauroux I;Grelac F;Carpentier W;Lokajczyk A;Gandrille S;Colliec-Jouault S;Fischer AM;Helley D
通讯作者:
Helley D
影响因子:
9.8
作者:
Benslimane-Ahmim, Zahia;Poirier, Florence;Boisson-Vidal, Catherine
通讯作者:
Boisson-Vidal, Catherine
影响因子:
20.3
作者:
Au, Patrick;Daheron, Laurence M.;Jain, Rakesh K.
通讯作者:
Jain, Rakesh K.
DOI:
10.1083/jcb.139.1.265
发表时间:
1997-10-06
期刊:
The Journal of cell biology
影响因子:
--
作者:
Bloch W;Forsberg E;Lentini S;Brakebusch C;Martin K;Krell HW;Weidle UH;Addicks K;Fässler R
通讯作者:
Fässler R