Recovery from hind limb ischemia is less effective in type 2 than in type 1 diabetic mice: Roles of endothelial nitric oxide synthase and endothelial progenitor cells

Yan, Jinglian; Tie, Guodong; Park, Brian; Yan, Yagai; Nowicki, Philip T.; Messina, Louis M.

doi:10.1016/j.jvs.2009.08.007

Cited by 93 publications

(104 citation statements)

References 37 publications

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“…Moreover, blood flow recovery was significantly less within type 2 diabetic mice compared to type 1 diabetic group [61]. These findings lend further support that other components including, hyperlipidemia and obesity, contribute to the observed impaired blood flow in type 2 diabetes compared to type-1.…”

Section: Experimental Evidence Of CLI In Obesitysupporting

confidence: 72%

Cell Therapy and Critical Limb Ischemia: Evidence and Window of Opportunity in Obesity

Elshaer

Lorys

El-Remessy

2016

OCTOA

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Section: Experimental Evidence Of CLI In Obesitysupporting

confidence: 72%

Cell Therapy and Critical Limb Ischemia: Evidence and Window of Opportunity in Obesity

Elshaer

Lorys

El-Remessy

2016

OCTOA

View full text Add to dashboard Cite

“…The decrease in vascularization in diabetic animals is in line with other studies. Decelerated neoangiogenesis was reported in the ischemic hindlimb model of diabetic mice [11,37]. Thereby the possible mechanisms underlying impaired neovascularization in the diabetic organism are highly diverse.…”

Section: Discussionmentioning

confidence: 99%

“…A potential disadvantage could be the mutation of the leptin receptor. Leptin influences the proinflammatory immune response [35] as well as T-cell functions [36], which could affect angiogenesis [11,37].…”

Section: Discussionmentioning

confidence: 99%

“…Thereby the possible mechanisms underlying impaired neovascularization in the diabetic organism are highly diverse. Some of these mechanisms involve dysfunctioning and decrease in the number of endothelial progenitor cells [37]. Considerably increased differentiation of MSCs to adipocytes may be another reason for the reduced angiogenic capacity [37].…”

Section: Discussionmentioning

confidence: 99%

“…Some of these mechanisms involve dysfunctioning and decrease in the number of endothelial progenitor cells [37]. Considerably increased differentiation of MSCs to adipocytes may be another reason for the reduced angiogenic capacity [37]. Concerning diabetic microangiopathy the thickening of the basement membrane has to be considered [49].…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Decelerated vascularization in tissue-engineered constructs in association with diabetes mellitus in vivo

Schumann¹,

Lindhorst²,

Kampmann³

et al. 2015

Journal of Diabetes and its Complications

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Experimental peripheral arterial disease: new insights into muscle glucose uptake, macrophage, and T-cell polarization during early and late stages

et al. 2014

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Peripheral arterial disease (PAD) is a common disease with increasing prevalence, presenting with impaired walking ability affecting patient's quality of life. PAD epidemiology is known, however, mechanisms underlying functional muscle impairment remain unclear. Using a mouse PAD model, aim of this study was to assess muscle adaptive responses during early (1 week) and late (5 weeks) disease stages. Unilateral hindlimb ischemia was induced in ApoE−/− mice by iliac artery ligation. Ischemic limb perfusion and oxygenation (Laser Doppler imaging, transcutaneous oxygen pressure assessments) significantly decreased during early and late stage compared to pre‐ischemia, however, values were significantly higher during late versus early phase. Number of arterioles and arteriogenesis‐linked gene expression increased at later stage. Walking ability, evaluated by forced and voluntary walking tests, remained significantly decreased both at early and late phase without any significant improvement. Muscle glucose uptake ([18F]fluorodeoxyglucose positron emission tomography) significantly increased during early ischemia decreasing at later stage. Gene expression analysis showed significant shift in muscle M1/M2 macrophages and Th1/Th2 T cells balance toward pro‐inflammatory phenotype during early ischemia; later, inflammatory state returned to neutrality. Muscular M1/M2 shift inhibition by a statin prevented impaired walking ability in early ischemia. High‐energy phosphate metabolism remained unchanged (31‐Phosphorus magnetic resonance spectroscopy). Results show that rapid transient muscular inflammation contributes to impaired walking capacity while increased glucose uptake may be a compensatory mechanisms preserving immediate limb viability during early ischemia in a mouse PAD model. With time, increased ischemic limb perfusion and oxygenation assure muscle viability although not sufficiently to improve walking impairment. Subsequent decreased muscle glucose uptake may partly contribute to chronic walking impairment. Early inflammation inhibition and/or late muscle glucose impairment prevention are promising strategies for PAD management.

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Recovery from hind limb ischemia is less effective in type 2 than in type 1 diabetic mice: Roles of endothelial nitric oxide synthase and endothelial progenitor cells

Cited by 93 publications

References 37 publications

Cell Therapy and Critical Limb Ischemia: Evidence and Window of Opportunity in Obesity

Cell Therapy and Critical Limb Ischemia: Evidence and Window of Opportunity in Obesity

Decelerated vascularization in tissue-engineered constructs in association with diabetes mellitus in vivo

Experimental peripheral arterial disease: new insights into muscle glucose uptake, macrophage, and T-cell polarization during early and late stages

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