Induction of cardiovascular pathology in a novel model of low-grade chronic inflammation

Smith, Brenda J.; Lightfoot, Stan; Lerner, Megan R.; Denson, Kent D.; Morgan, Daniel L.; Hanas, Jay S.; Bronze, Michael S.; Postier, Russell G.; Brackett, Daniel J.

doi:10.1016/j.carpath.2007.07.011

Cited by 31 publications

(22 citation statements)

References 63 publications

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“…Continuous administration of LPS significantly stimulated innate immune responses characterized by an elevation of lymphocytes, neutrophils, and eosinophils. Such a detrimental effect of LPS on myocardium (as shown in increased innate immune responses) in female rats has been reported previously [21]. Our data show that circulating WBC, lymphocytes, neutrophils, and eosinophils were significantly suppressed by GTP supplementation in LPS-treated rats.…”

Section: Discussionsupporting

confidence: 71%

Green tea polyphenols avert chronic inflammation-induced myocardial fibrosis of female rats

et al. 2011

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Section: Discussionsupporting

confidence: 71%

Green tea polyphenols avert chronic inflammation-induced myocardial fibrosis of female rats

et al. 2011

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“…The novel AAASP concept provides an explanation for observation that the arterial wall of younger animals in response to experimental induction of low-grade chronic inflammation, e.g., by hypertension or early atherosclerosis, is transformed into a phenotype that is strikingly similar to that which develops during aging [3**, 4, 63]. Thus, “aging”-associated arterial changes and those associated with hypertension and atherosclerosis are fundamentally intertwined at the cellular and molecular levels (Table 1) [3**].…”

Section: Resultsmentioning

confidence: 99%

Arterial aging: a journey into subclinical arterial disease

Wang

Monticone

Lakatta

2010

Current Opinion in Nephrology and Hypertension

148

150

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Purpose-Age-associated arterial alterations in cells, matrix, and biomolecules are the foundation for the initiation and progression of cardiovascular diseases in older persons. This review focuses on the latest advances on the intertwining of aging and disease within the arterial wall at the cell and molecular levels.Recent findings-Endothelial dysfunction, VSMC proliferation/invasion/secretion, matrix fragmentation, collagenization and glycation are characteristics of an age-associated arterial phenotype that creates a microenvironment enriched with reactive oxygen species (ROS) for the pathogenesis of arterial disease. This niche creates an age-associated arterial secretory phenotype (AAASP), which is orchestrated by the concerted effects of numerous age-modified Ang II signaling molecules. Most of these biomolecular, cell, and matrix modifications that comprise the AASP can be elicited by experimental hypertension or atherosclerosis at a younger age. The arterial AAASP also shares features of a senescence associated secretory phenotype (SASP) identified in other mesenchymocytes, i.e. fibroblasts.Summary-A subclinical AAASP evolves during aging. Targeting this subclinical AAASP may reduce the incidence and progression of the quintessential age-associated arterial diseases, i.e. hypertension and atherosclerosis.

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“…Endotoxemia has been linked to the development of low-grade systemic inflammation and vascular inflammation via toll-like receptor-dependent mechanisms (85). In obese individuals, intestinal microbiota composition was associated with local and systemic inflammation (elevated C-reactive protein) (86).…”

Section: Hypertension and The Microbiomementioning

confidence: 99%

The Microbiome and Blood Pressure: Can Microbes Regulate Our Blood Pressure?

2017

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The surfaces of the human body are heavily populated by a highly diverse microbial ecosystem termed the microbiota. The largest and richest among these highly heterogeneous populations of microbes is the gut microbiota. The collection of microbes and their genes, called the microbiome, has been studied intensely through the past few years using novel metagenomics, metatranscriptomics, and metabolomics approaches. This has enhanced our understanding of how the microbiome affects our metabolic, immunologic, neurologic, and endocrine homeostasis. Hypertension is a leading cause of cardiovascular disease worldwide; it contributes to stroke, heart disease, kidney failure, premature death, and disability. Recently, studies in humans and animals have shown that alterations in microbiota and its metabolites are associated with hypertension and atherosclerosis. In this review, we compile the recent findings and hypotheses describing the interplay between the microbiome and blood pressure, and we highlight some prospects by which utilization of microbiome-related techniques may be incorporated to better understand the pathophysiology and treatment of hypertension.

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Induction of cardiovascular pathology in a novel model of low-grade chronic inflammation

Cited by 31 publications

References 63 publications

Green tea polyphenols avert chronic inflammation-induced myocardial fibrosis of female rats

Green tea polyphenols avert chronic inflammation-induced myocardial fibrosis of female rats

Arterial aging: a journey into subclinical arterial disease

The Microbiome and Blood Pressure: Can Microbes Regulate Our Blood Pressure?

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