Angiotensin Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers (ACEI/ARB) are Associated with Improved Limb Salvage after Infrapopliteal Interventions for Critical Limb Ischemia.
Elevated expression of CXCR7 enhances EPC resistance to diabetes mellitus-induced oxidative damage and improves therapeutic efficacy of EPCs in treating diabetic limb ischemia.
A total of 25 diabetic patients with CLI treated in our foot clinic during the period 2008-2014 with ACT generating potential vasculogenesis were consecutively included in the study; 14 diabetic patients with CLI who underwent PTA during the same period were included in a control group in which no vasculogenesis had occurred.
A total of 25 diabetic patients with CLI treated in our foot clinic during the period 2008-2014 with ACT generating potential vasculogenesis were consecutively included in the study; 14 diabetic patients with CLI who underwent PTA during the same period were included in a control group in which no vasculogenesis had occurred.
A total of 25 diabetic patients with CLI treated in our foot clinic during the period 2008-2014 with ACT generating potential vasculogenesis were consecutively included in the study; 14 diabetic patients with CLI who underwent PTA during the same period were included in a control group in which no vasculogenesis had occurred.
A total of 25 diabetic patients with CLI treated in our foot clinic during the period 2008-2014 with ACT generating potential vasculogenesis were consecutively included in the study; 14 diabetic patients with CLI who underwent PTA during the same period were included in a control group in which no vasculogenesis had occurred.
In this study, we assessed the potential of a new angiogenic factor AGGF1 for therapeutic angiogenesis in a critical limb ischemia model in mice for PAD.
This study explored the impact of UA on endothelial cell (EC) activities in vitro in HCECs, vascular neovasculogenesis in vivo in a mouse hind limb ischemia model, and the possible role of AIF-1 in vasculogenesis.
These results suggest that E6E7-MSCs increase the ability to secrete angiogenic factors via AKT activation, and E6E7-CM is abundant in IL-1β and VEGFA levels and thereby increases the ability to improve blood perfusion and prohibit muscle loss or fibrosis in a mouse limb ischemia model.
The 2005-2012 National Surgical Quality Improvement Program was analyzed to determine associated complications, mortality, length of stay (LOS), and readmissions for patients with hypoalbuminemia (serum albumin <3.5 g/dL and <2.8 g/dL) undergoing infrainguinal lower extremity bypass for critical limb ischemia.
Univariate analysis revealed shorter ECMO duration, higher body mass index, preimplantation creatinine > 100 mmol/l, lower preimplantation serum albumin, and the development of stroke or limb ischemia on ECMO to be significantly associated with mortality while on ECMO.
Activation of Src and αPix were also compromised at least to some extent in 12/15-Lox(-/-) mice compared with WT mice in response to hind-limb ischemia.
We examined the impacts of combinatorial Ang-1 gene transfer and low-dose autologous BM-MNC implantation on therapeutic angiogenesis in a rabbit model of hind limb ischemia.
Among LEPAD patients, those with critical limb ischemia (n=43) showed higher AGF levels (124.9±73.9 vs. 88.98±53.26ng/mL, P=0.01) compared with those with intermittent claudication (n=62).
Our goal was to determine whether AGF enhances blood flow in a mouse hind-limb ischemia model and to define molecular mechanisms underlying AGF signaling in endothelial cells.
In this study, green fluorescent protein-expressing ADRCs (GFP-ADRCs) were obtained, labeled with acetylated 3-aminopropyltrimethoxysilane (APTS)-coated iron oxide nanoparticles (APTS NPs), and injected into an old apolipoprotein E knockout (ApoE-KO) mouse model with hind limb ischemia.
When iPS-ECs overexpressing FSTL3 were subcutaneously injected in in vivo angiogenic model or intramuscularly injected in a hind limb ischemiaNOD.CB17-Prkdcscid/NcrCrl SCID mice model, FSTL3 significantly induced angiogenesis and blood flow recovery, respectively.
When injected systemically into wild-type mice with unilateral limb ischemia, bone marrow MNCs from syngenic B(2)R-deficient mice resulted in reduced homing of sca-1(+) and cKit(+)flk1(+) progenitors to ischemic muscles, impaired reparative neovascularization, and delayed perfusion recovery as compared with wild-type MNCs.
Hind-limb ischemia was surgically induced in Bach1(-/-) mice and their wild-type littermates and in C57BL/6J mice treated with adenoviruses coding for Bach1 or GFP.
We explored (i) if EZH2 expression is regulated by hypoxia and ischemia; (ii) the impact of EZH2 on the expression of two pro-angiogenic genes: eNOS and BDNF; (iii) the functional effect of EZH2 inhibition on cultured endothelial cells (ECs); (iv) the therapeutic potential of EZH2 inhibition in a mouse model of limb ischemia (LI).