Atherosclerosis: humoral and cellular factors of inflammation

Langheinrich, AC; Bohle, Rainer M.

doi:10.1007/s00428-004-1180-4

Cited by 33 publications

(20 citation statements)

References 73 publications

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“…In addition, lipocortin 1 (or annexin 1), as mentioned above for macrophages, is also produced by granulocytes (54). Finally, granulocytes are associated with capillary closure in spontaneously diabetic monkey retinas (55), and granulocytes might play a role in atherosclerosis (56).…”

Section: Fig 1 Islet Fibrosis Progresses Rapidly In Mild Hyperglycementioning

confidence: 99%

Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat

Homo‐Delarche

Caldérari

Irminger³

et al. 2006

Diabetes

188

180

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The molecular pathways leading to islet fibrosis in diabetes are unknown. Therefore, we studied gene expression in islets of 4-month-old Goto-Kakizaki (GK) and Wistar control rats. Of 71 genes found to be overexpressed in GK islets, 24% belong to extracellular matrix (ECM)/cell adhesion and 34% to inflammatory/immune response families. Based on gene data, we selected several antibodies to study fibrosis development during progression of hyperglycemia by immunohistochemistry. One-month-old GK and Wistar islets appeared to be similar. Two-month-old GK islets were strongly heterogenous in terms of ECM accumulation compared with Wistar islets. GK islet vascularization, labeled by von Willebrand factor, was altered after 1 month of mild hyperglycemia. Numerous macrophages (major histocompatibility complex class II ؉ and CD68 ؉ ) and granulocytes were found in/around GK islets. These data demonstrate that marked inflammatory reaction accompanies GK islet fibrosis and suggest that islet alterations in this nonobese model of type 2 diabetes develop in a way reminiscent of microangiopathy. Diabetes 55: [1625][1626][1627][1628][1629][1630][1631][1632][1633] 2006

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Section: Fig 1 Islet Fibrosis Progresses Rapidly In Mild Hyperglycementioning

confidence: 99%

Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat

Homo‐Delarche

Caldérari

Irminger³

et al. 2006

Diabetes

188

180

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“…For instance, autopsies of Egyptian mummies found atherosclerotic plaques in a majority of this sample (16͞24) (15,16). As early as 1858, Virchow concluded that ''an inflammation of the arterial coat was the starting point of the so-called atheromatous degeneration'' (17).…”

mentioning

confidence: 99%

Infection, inflammation, height, and longevity

Crimmins

Finch²

2005

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

408

316

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Using historical data from cohorts born before the 20th century in four northern European countries, we show that increasing longevity and declining mortality in the elderly occurred among the same birth cohorts that experienced a reduction in mortality at younger ages. Concurrently, these cohorts also experienced increasing adult height. We hypothesize that both the decline in old-age mortality and the increase in height were promoted by the reduced burden of infections and inflammation. Thus, early growth and cardiovascular diseases of old age may share infectious and inflammatory causes rooted in the external environment.aging ͉ vascular disease ͉ mortality ͉ historical cohorts L ife expectancy has doubled during the last 250 years from preindustrial norms of 35-40 years (1, 2). Although all ages have benefited, the increases among the elderly began many decades after the increases at younger ages (3). We have hypothesized that the historical increase in life expectancy at the older ages was due in part to life-long reduction in exposure to chronic inflammation (4). It is well known that the survivors of birth cohorts with lowered early age mortality due to infections experienced lower mortality throughout adult life (5-8), a relationship we have characterized as the ''cohort morbidity phenotype'' (4). Others have proposed that mortality at young and old age is linked by improvements in nutrition and a reduction in organ damage due to infections (9,10). We add the reduction in lifelong exposure to inflammation to these explanations and develop in more detail the physiological mechanisms linking lifetime exposure to infections and late life health outcomes. We also consider inflammation as a possible link between childhood mortality and adult height (11).We argue that the demographic and economic revolutions beginning Ͼ200 years ago were accompanied by a physiological revolution, which occurred long before the benefits of modern medicine. The historical reduction in inflammation was an internal manifestation of the physiological revolution, which was also indexed by the historical increases in height. We propose a general model in which the reduction in lifelong levels of infections and inflammation reduced and delayed the atherosclerotic process and mortality due to heart disease and allowed increased height (Fig. 1). This heuristic model emphasizes the pathway from decreases in infection through reductions in inflammation but recognizes that other potential links include improvements in diet and nutrition and reductions in direct organ damage. Thus, our model considers a broader set of pathophysiological mechanisms linking health across the life course than presented heretofore.Extensive debate over the causes of the historical mortality decline has not resolved the relative roles of improved public health, vaccines, income, and nutrition (1, 12). However, all of these factors would have reduced exposure to, resistance to, or consequences of infections. The role we hypothesize for inflammation considers the ...

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“…11 VV are generally not present in wild-type mice and they do not develop advanced atherosclerotic lesions, but apolipoprotein E (apoE) Ϫ/Ϫ /low-density lipoprotein (LDL) Ϫ/Ϫ double knockout mice develop lesions with considerable structural similarity to human atherosclerosis. 12 The present study was designed to characterize atherosclerotic lesions and the localization and time course of VV neovascularization and adventitial inflammation relative to growing plaques in apoE Ϫ/Ϫ / LDL Ϫ/Ϫ double knockout mice.…”

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confidence: 99%

Correlation of Vasa Vasorum Neovascularization and Plaque Progression in Aortas of Apolipoprotein E ^−/− /Low-Density Lipoprotein ^−/− Double Knockout Mice

Langheinrich

Michniewicz

Sedding

et al. 2006

ATVB

127

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Objective-We hypothesized that apolipoprotein E (apoE)Ϫ/Ϫ /low-density lipoprotein (LDL) Ϫ/Ϫ double knockout mice might develop vasa vasorum (VV) in association with advanced lesion formation. Methods and Results-Aortas from apoEϪ/Ϫ /LDL Ϫ/Ϫ mice aged 16, 18, 20, or 80 weeks were infused in situ with Microfil, harvested, and scanned with micro-computed tomography (CT). We characterized plaque volume and CT "density" as well as VV luminal volume along the aorta using Analyze 6.0 software. Results were complemented by a detailed histological plaque classification according to American Heart Association guidelines. From 16 to 80 weeks, plaque volume and VV opacified lumen volume increased with age (PϽ0.001). The 3-dimensional micro-CT images of arterial and venous VV trees allowed perfusion territories to be delineated. The spatial location and magnitude of VV density and adventitial inflammation were strongly correlated in advanced atherosclerotic lesions (rϭ0.91) and identified as an independent correlate to advanced lesions. At age 80 weeks, VV luminal volume was increased 20-fold compared with animals at age 16 weeks (PϽ0.001). Micro-CT showed that adventitial VV communicate with intraplaque microvessels. Conclusion-Our

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Atherosclerosis: humoral and cellular factors of inflammation

Cited by 33 publications

References 73 publications

Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat

Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat

Infection, inflammation, height, and longevity

Correlation of Vasa Vasorum Neovascularization and Plaque Progression in Aortas of Apolipoprotein E ^−/− /Low-Density Lipoprotein ^−/− Double Knockout Mice

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Atherosclerosis: humoral and cellular factors of inflammation

Cited by 33 publications

References 73 publications

Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat

Islet Inflammation and Fibrosis in a Spontaneous Model of Type 2 Diabetes, the GK Rat

Infection, inflammation, height, and longevity

Correlation of Vasa Vasorum Neovascularization and Plaque Progression in Aortas of Apolipoprotein E −/− /Low-Density Lipoprotein −/− Double Knockout Mice

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Correlation of Vasa Vasorum Neovascularization and Plaque Progression in Aortas of Apolipoprotein E ^−/− /Low-Density Lipoprotein ^−/− Double Knockout Mice