Insulin Signaling in Arteries Prevents Smooth Muscle Apoptosis

Nakazawa, Toru; Chiba, Tsuyoshi; Kaneko, Eiji; Yui, Katsumasa; Yoshida, Masayuki; Shimokado, Kentaro

doi:10.1161/01.atv.0000158307.66945.b4

Cited by 22 publications

(11 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, the simultaneous insult of hyperglycaemia and hyperlipidaemia induced formation of matrix vesicles and of apoptotic bodies that both may serve as calcification matrices. These results complete earlier observations that under diabetic conditions SMCs were more susceptible to cell death, a condition to which additional apoptosis-inducing factors contribute, such as AGEs and free radicals (Nakazawa et al, 2005).…”

Section: Smcs Dysfunction In Hyperlipidaemia: Migration and Proliferasupporting

confidence: 90%

Arterial smooth muscle cells dysfunction in hyperglycaemia and hyperglycaemia associated with hyperlipidaemia: from causes to effects

Popov¹,

Constantinescu²

2008

Archives of Physiology and Biochemistry

View full text Add to dashboard Cite

Given the important role of smooth muscle cells in arterial wall dysfunction in diabetes, as well as in diabetes associated with accelerated atherosclerosis, we provide a brief review of the recent achievements in identification of signalling molecules underlying their altered cellular responses, and examine the consequences of these pathological insults on smooth muscle cells properties. The original results emerging from the Golden Syrian hamster model (rendered diabetic or simultaneously hyperlipidaemic-diabetic) and from human aortic smooth muscle cells cultured in 25 mM glucose (to mimic diabetic condition) or sera of obese type 2 diabetic patients (to mimic the metabolic syndrome condition) are presented in this context. We conclude this review with several open issues disclosed by the most recent literature that deserve essential attention for targeting the translational medicine.

show abstract

Section: Smcs Dysfunction In Hyperlipidaemia: Migration and Proliferasupporting

confidence: 90%

Arterial smooth muscle cells dysfunction in hyperglycaemia and hyperglycaemia associated with hyperlipidaemia: from causes to effects

Popov¹,

Constantinescu²

2008

Archives of Physiology and Biochemistry

View full text Add to dashboard Cite

show abstract

“…MMPs represent a marker of vascular disease (Maxwell et al 2001), as was also demonstrated by our group in children and adolescents with type-1 diabetes (Derosa et al 2004) and in patients with hypertension (Derosa et al 2006) and pathological conditions associated with chronic endothelial dysfunction and unstable plaque formation (Nakazawa et al 2005).…”

Section: Discussionsupporting

confidence: 55%

Metalloproteinases in Diabetics and Nondiabetics during Acute Coronary Syndromes and after 3 Months

Derosa

Cicero

Scalise³

et al. 2007

Endothelium

View full text Add to dashboard Cite

The authors hypothesized that matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1, and TIMP-2 would be abnormal in acute coronary syndromes (ACS). Forty-six diabetic and 78 nondiabetic patients during ACS and after 3 months were enrolled in this study. MMP-2, -9 and TIMP-1, -2 plasma levels were measured. Significant decrease of MMP-2, TIMP-1, and TIMP-2 plasma levels was observed in the nondiabetic group with ACS after 3 months compared to the baseline value. Significant decrease of MMP-2, MMP-9, TIMP-1, and TIMP-2 plasma levels was observed in the diabetic group with ACS after 3 months compared to the baseline value. MMP-9, TIMP-1, and TIMP-2 plasma levels were higher in diabetic patients during ACS compared to nondiabetic patients during ACS. TIMP-1 and TIMP-2 increases were observed in diabetic patients with ACS at 3 months compared to nondiabetic patients after ACS. MMPs and TIMP-1 and -2 plasma levels were alterated in nondiabetic and diabetic patients during ACS and after 3 months, which may reflect abnormal extracellular matrix metabolism in diabetes during and after acute event.

show abstract

“…Insulin exerts antiapoptotic effects in macrophages, endothelial cells, and smooth muscle cells in vitro. [61][62][63] During phagocytosis of apoptotic cells, both PI3K/ AKT 64,65 and MEK/ERK [65][66][67] signaling cascades in normal phagocytic macrophages are involved. Further research is needed to determine whether engulfment of apoptotic cells by macrophages is altered in type 2 diabetes.…”

Section: Potential Mechanisms: Role Of Macrophage Apoptosis and Phagomentioning

confidence: 99%

The Macrophage at the Crossroads of Insulin Resistance and Atherosclerosis

Liang

Han

Senokuchi

et al. 2007

Circulation Research

123

105

View full text Add to dashboard Cite

Abstract-The macrophage has emerged as an important player in the pathogenesis of both atherosclerosis and insulin resistance. Cross-talk between inflammatory macrophages and adipocytes may be involved in insulin resistance in peripheral tissues. Defective insulin signaling in cells of the arterial wall including macrophages may promote the development of atherosclerosis. Insulin resistant macrophages are more susceptible to endoplasmic reticulum stress and apoptosis in response to various stimuli such as nutrient deprivation, free cholesterol loading, and oxidized LDL.

show abstract

Insulin Signaling in Arteries Prevents Smooth Muscle Apoptosis

Cited by 22 publications

References 45 publications

Arterial smooth muscle cells dysfunction in hyperglycaemia and hyperglycaemia associated with hyperlipidaemia: from causes to effects

Arterial smooth muscle cells dysfunction in hyperglycaemia and hyperglycaemia associated with hyperlipidaemia: from causes to effects

Metalloproteinases in Diabetics and Nondiabetics during Acute Coronary Syndromes and after 3 Months

The Macrophage at the Crossroads of Insulin Resistance and Atherosclerosis

Contact Info

Product

Resources

About