Multifactorial treatment increases endothelial progenitor cells in patients with type 2 diabetes

Reinhard, Henrik; Jacobsen, Peter Karl; Lajer, Maria; Pedersen, Nadja; Billestrup, Nils; Mandrup-Poulsen, Thomas; Parving, Hans‐Henrik; Rossing, Peter

doi:10.1007/s00125-010-1843-4

Cited by 35 publications

(27 citation statements)

References 14 publications

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“…Enrolling 74 patients with type Ⅰ diabetes, EPCs counts were significantly lower in these patients compared to 80 healthy controls [62] . Similarly, other studies have also demonstrated that EPCs levels were lower in patients with diabetes mellitus type Ⅱ compared to healthy controls [63][64][65] . Treatment with strict glycemic control and total cholesterol improvement increased EPCs numbers [65] .…”

Section: Epcs and Diabetesmentioning

confidence: 58%

“…Similarly, other studies have also demonstrated that EPCs levels were lower in patients with diabetes mellitus type Ⅱ compared to healthy controls [63][64][65] . Treatment with strict glycemic control and total cholesterol improvement increased EPCs numbers [65] . There is strong evidence that patients with diabetes types Ⅰ and Ⅱ appear to have lower EPCs numbers compared to healthy controls.…”

Section: Epcs and Diabetesmentioning

confidence: 58%

“…Despite the significant experimental study of Laufs et al [101] , Luk et al [109] showed that there was no significant increase in CD34/KDR + EPCs after an 8-wk exercise training programme on 32 patients with CAD compared to controls. In contrast, in a recent uncontrolled study by [34,35] [34-36] ↑ EPC levels in acute exacerbation [36] ↑ Late apoptotic progenitors [35] ↓ EPC levels in advanced stages [34,35] LVADs ↑ EPC levels [38,39] PAH ↑ EPC levels [42,45,46] Conflicting results [43,44] Critical illness ↑ EPC levels in sepsis and septic shock [47,49] [ [47][48][49] ↑ EPC levels in early acute lung injury [48] COPD ↑ EPC levels [52] Conflicting results [53,54] ↑ EPC levels in exacerbation of COPD [55] ↓ EPC mobilization and colonyforming capacity [56] OSA ↑ EPC levels [58,60] Conflicting results [59] -No difference [57] Diabetes mellitus type Ⅰand Ⅱ ↓ EPC levels [61][62][63][64][65] Cerebrovascular disease ↓ EPC levels in stroke [66] [66-69] -No difference in ischemic stroke [67] ↑ EPC levels in acute ischemic stroke [67] ↓ EPC levels in atherothrombotic cerebral ischemic event [68] ↓ EPC colony forming in acute stroke [69] PAD ↑ EPC levels in moderate phase [71,72] ↑ EPC levels in adva...…”

Section: Effects Of Exercise Training On Epcsmentioning

confidence: 99%

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Circulating endothelial and progenitor cells: Evidence from acute and long-term exercise effects

Koutroumpi¹

2012

WJC

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Circulating bone-marrow-derived cells, named endothelial progenitor cells (EPCs), are capable of maintaining, generating, and replacing terminally differentiated cells within their own specific tissue as a consequence of physiological cell turnover or tissue damage due to injury. Endothelium maintenance and restoration of normal endothelial cell function is guaranteed by a complex physiological procedure in which EPCs play a significant role. Decreased number of peripheral blood EPCs has been associated with endothelial dysfunction and high cardiovascular risk. In this review, we initially report current knowledge with regard to the role of EPCs in healthy subjects and the clinical value of EPCs in different disease populations such as arterial hypertension, obstructive sleep-apnea syndrome, obesity, diabetes mellitus, peripheral arterial disease, coronary artery disease, pulmonary hypertension, and heart failure. Recent studies have introduced the novel concept that physical activity, either performed as a single exercise session or performed as part of an exercise training program, results in a significant increase of circulating EPCs. In the second part of this review we provide preliminary evidence from recent studies investigating the effects of acute and long-term exercise in healthy subjects and athletes as well as in disease populations.

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Section: Epcs and Diabetesmentioning

confidence: 58%

Section: Epcs and Diabetesmentioning

confidence: 58%

Section: Effects Of Exercise Training On Epcsmentioning

confidence: 99%

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Circulating endothelial and progenitor cells: Evidence from acute and long-term exercise effects

Koutroumpi¹

2012

WJC

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“…86 In addition, a combination of statin and angiotensin receptor blocker seems to have a synergistic effect to increase the number and function of EPCs in DM. 85,87 Lifestyle modifications, including exercise 88 and weight reduction, 89 have also been shown to increase EPC number and function in patients with cardiovascular disease or DM.…”

Section: Approaches To Improve Epc Function and Survivalmentioning

confidence: 99%

Specific Role of Impaired Glucose Metabolism and Diabetes Mellitus in Endothelial Progenitor Cell Characteristics and Function

Yiu

Tse

2014

ATVB

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Abstract-The disease burden of diabetes mellitus (DM) and its associated cardiovascular complications represent a growing and major global health problem. Recent studies suggest that circulating exogenous endothelial progenitor cells (EPCs) play an important role in endothelial repair and neovascularization at sites of injury or ischemia. 1 This has been attributed to the occurrence of endothelial dysfunction that leads to the initiation and progression of atherosclerotic vascular disease 2 and impaired neovascularization after ischemia induced by hyperglycemia. 3,4 In patients with impaired glucose metabolism and DM, the vascular endothelium is challenged by inflammation, reactive oxygen species, and deletion of endothelial nitric oxide synthase (eNOS) with resultant endothelial dysfunction.2,5-7 The depletion and dysfunction of the circulating endothelial progenitor cells (EPCs) are thought to underlie the endothelial dysfunction in DM. In this review, the possible mechanisms, functional consequences, and the potential therapeutic approach for impaired EPCs in DM are discussed. A systematic literature search for full-text papers in the English language was performed using MEDLINE, Embase, and the Cochrane library through to February 2014. In the search phrases used, the following terms were combined with the phrase AND Diabetes: endothelial progenitor cells, cardiovascular disease, myocardial infarction, and stroke.

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“…In general the bone marrowderived EPCs in the diabetic patients are considered as dysfunctional, producing fewer endothelial cells and with reduced replicative and migratory potential [103]. As to fully divert the physiological role of EPCs in tissue repair and angiogenesis, the duet hyperglycemia-ROS stimulate the EPCs to produce pro-inflammatory cytokines and to shift NO production by elevating i-NOS and decreasing e-NOS [104]. As described for other cells, AGEs treatment disrupts EPCs physiology thus leading to a downregulation of e-NOS and Bcl-2 expression, as well as an elevation in cyclo-oxygenase-2, Bax, NF-ĸB, and caspase-3 in a MAPK (ERK/P38/JNK)-dependant manner [105].…”

Section: Diabetic Wound Endothelial Cellsmentioning

confidence: 99%

Type 2 Diabetes Mellitus (T2DM): Biological Overview from Pathways to Organelles and its Translation toward a Torpid Wound Healing Process

Guillen-Nieto¹,

Herrera-Martínez²

2013

J Diabetes Metab

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T2DM is a heterogeneous group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Hyperglycemia may simply represent the tip of a broad series of molecular events from mitochondrial damages, to epigenetic and metabolic pathways deregulations. At the same time, hyperglycemia appears as the most proximal trigger for the onset and perpetual progression of multi-organ complications even under normoglycemic conditions. Thus, the initial hyperglycemic hit translates into a permanently harmful cellular imprinting as has been demonstrated in diabetic donors' cells after several passages and cultured in ideal conditions. The wound healing failure along with the inability of the innate immunity to control peripheral infections is the hybrid that determines that 85% of all non-traumatic lower extremity amputations are practiced in diabetic subjects. Diabetic wounds exhibit a complex networking of inflammatory cytokines, local proteases, cytotoxic reactive oxygen and nitrogen species and a polymicrobial biofilm that impose a stagnant phenotype. All these ingredients negatively impact on fibroblasts, endothelial cells and keratinocytes while paradoxically perpetuate the immuno-inflammatory infiltrate. Although the molecular fundamentals toward chronification have not been elucidated, it seems that different gene simultaneously converge to impose the wound cells a pro-senescent, pro-catabolic and pro-apoptotic phenotype given the lack of a "physiological tuning" of tyrosine kinase-dependent receptors due to their limited activation by insulin and local growth factors. Although recombinant growth factors and smart devices have been introduced during the last years the figures of amputations are still discouraging. Faults have been committed while selecting the appropriate growth factor and because of the "chronic" instinct to treat the chronic wounds topically, where bioavailability of the active principle is compromised by wound and bacterial biofilm proteases. The periodic intralesional infiltration of epidermal growth factor has proved to overcome this hurdle. Granulation tissue growth stimulation and wound healing capacity has been restored in diabetic patients by this procedure in several clinical trials and common clinical practice studies.

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Multifactorial treatment increases endothelial progenitor cells in patients with type 2 diabetes

Cited by 35 publications

References 14 publications

Circulating endothelial and progenitor cells: Evidence from acute and long-term exercise effects

Circulating endothelial and progenitor cells: Evidence from acute and long-term exercise effects

Specific Role of Impaired Glucose Metabolism and Diabetes Mellitus in Endothelial Progenitor Cell Characteristics and Function

Type 2 Diabetes Mellitus (T2DM): Biological Overview from Pathways to Organelles and its Translation toward a Torpid Wound Healing Process

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