Morphological characteristics of coronary atherosclerosis in diabetes mellitus

Virmani, Renu; Burke, Allen; Kolodgie, Frank D.

doi:10.1016/s0828-282x(06)70991-6

Cited by 86 publications

(68 citation statements)

References 23 publications

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“…Our preliminary data showed that oxidized LDL reduced MCP-1-mediated chemotaxis compared with LDL, a result compatible with previous reports showing that oxidized LDL caused a rapid reduction of CCR2 expression in monocytes, rendering these cells non-responsive to MCP-1 [25,37]. Our findings suggest differing cellular responses to AGE-LDL and oxidized LDL.…”

Section: Discussionsupporting

confidence: 91%

“…Targeted inactivation of either the MCP-1 or the CCR2 gene markedly decreased lesion formation in apoE-deficient mice [23], indicating that CCR2 engagement contributes to the development of atherosclerotic lesions. In particular, atheromata from diabetic patients have accentuated accumulation of macrophages, although the mechanisms remain unknown [24,25]. This study demonstrates that AGE-LDL increases CCR2 expression in human macrophages and stimulates MCP-1-mediated THP-1 monocytoid cell chemotaxis.…”

mentioning

confidence: 77%

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Glycated LDL increases monocyte CC chemokine receptor 2 expression and monocyte chemoattractant protein-1-mediated chemotaxis

et al. 2008

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Section: Discussionsupporting

confidence: 91%

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confidence: 77%

Glycated LDL increases monocyte CC chemokine receptor 2 expression and monocyte chemoattractant protein-1-mediated chemotaxis

et al. 2008

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“…Advanced plaques also contain molecules or conditions that promote calcium-based ER stress, including atherogenic lipoproteins and peroxynitrite (8,13), and lesional macrophages display multiple markers of UPR activation in vivo (9,10). Moreover, we recently found that the apoptosis pathway described here is enhanced in insulin-resistant macrophages both in vitro and in advanced atherosclerotic lesions, and the advanced lesions of humans with type II diabetes are characterized by increased lesional macrophage death and plaque necrosis (48,49). Thus, PRR-mediated macrophage apoptosis in advanced atherosclerotic lesions may be relevant particularly in the setting of insulin resistance.…”

Section: Discussionmentioning

confidence: 73%

Combinatorial pattern recognition receptor signaling alters the balance of life and death in macrophages

Seimon

Obstfeld²,

Moore³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

166

194

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Macrophage pattern recognition receptors (PRRs) play key roles in innate immunity, but they also may contribute to disease processes under certain pathological conditions. We recently showed that engagement of the type A scavenger receptor (SRA), a PRR, triggers JNK-dependent apoptosis in endoplasmic reticulum (ER)-stressed macrophages. In advanced atherosclerotic lesions, the SRA, activated JNK, and ER stress are observed in macrophages, and macrophage death in advanced atheromata leads to plaque necrosis. Herein, we show that SRA ligands trigger apoptosis in ER-stressed macrophages by cooperating with another PRR, Tolllike receptor 4 (TLR4), to redirect TLR4 signaling from prosurvival to proapoptotic. Common SRA ligands activate both TLR4 signaling and engage the SRA. The TLR4 effect results in activation of the proapoptotic MyD88-JNK branch of TLR4, whereas the SRA effect silences the prosurvival IRF-3-IFN-␤ branch of TLR4. The normal cell-survival effect of LPS-induced TLR4 activation is converted into an apoptosis response by immunoneutralization of IFN-␤, and the apoptosis effect of SRA ligands is converted into a cell-survival response by reconstitution with IFN-␤. Thus, combinatorial signaling between two distinct PRRs results in a functional outcomemacrophage apoptosis that does not occur with either PRR alone. PRR-induced macrophage death may play important roles in advanced atherosclerosis and in other innate immunity-related processes in which the balance between macrophage survival and death is critical.apoptosis ͉ atherosclerosis ͉ scavenger receptor ͉ Toll-like receptor ͉ innate immunity

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“…In previous autopsy studies, an extensive prevalence of necrotic core and inflammatory cells in coronary plaques was evident among diabetes subjects [29,30]. These findings may directly link to the increased risk in death [29,30], since these plaque features have been found as being at risk in plaque rupture associated with acute coronary syndrome and generally visualized as a part of non-calcified plaque on CCTA, especially LAP. Limited prior investigations have demonstrated the association between diabetes and plaque morphology and/or its progression.…”

Section: Discussionmentioning

confidence: 78%

Plaque progression assessed by a novel semi-automated quantitative plaque software on coronary computed tomography angiography between diabetes and non-diabetes patients: A propensity-score matching study

et al. 2016

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Plaque progression assessed by a novel semi-automated quantitative plaque software on coronary computed tomography angiography between diabetes and non-diabetes patients: A propensity-score matching study Methods: We identified 142 study subjects undergoing serial coronary computed tomography angiography. The resulting propensity score was applied 1:1 to match diabetic patients to non-diabetic patients for clinical risk factors, prior coronary stenting, coronary artery calcium (CAC) score and the serial scan interval, resulting in the 71 diabetes and 71 non-diabetes patients. Coronary plaque (total, calcified, noncalcified including fibrous, fibrous-fatty and low attenuation plaque [LAP]) volume normalized by total coronary artery length was measured using semi-automated plaque software and its change overtime between diabetic and non-diabetic patients was evaluated.Results: The matching was successful without significant differences between the two groups in all matched variables. The baseline volumes in each plaque also did not differ. During a mean scan interval of 3.4 ± 1.8 years, diabetic patients showed a 2-fold greater progression in normalized total plaque volume (TPV) than non-diabetes patients (52.8 mm 3 vs. 118.3 mm 3 , p ¼ 0.005). Multivariable linear regression model revealed that diabetes was associated with normalized TPV progression (b 72.3, 95%CI 24.3e120.3). A similar trend was observed for the non-calcified components, but not calcified plaque (b 3.8, 95%CI À27.0e34.7). Higher baseline CAC score was found to be associated with total, non-calcified and calcified plaque progression. However, baseline non-calcified volume but not CAC score was associated with LAP progression. Conclusions: The current study among matched patients indicates diabetes is associated with a greater plaque progression. Our results show the need for strict adherence of diabetic patients to the current preventive guidelines.

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Morphological characteristics of coronary atherosclerosis in diabetes mellitus

Cited by 86 publications

References 23 publications

Glycated LDL increases monocyte CC chemokine receptor 2 expression and monocyte chemoattractant protein-1-mediated chemotaxis

Glycated LDL increases monocyte CC chemokine receptor 2 expression and monocyte chemoattractant protein-1-mediated chemotaxis

Combinatorial pattern recognition receptor signaling alters the balance of life and death in macrophages

Plaque progression assessed by a novel semi-automated quantitative plaque software on coronary computed tomography angiography between diabetes and non-diabetes patients: A propensity-score matching study

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