Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Consumption of cow's milk and cow's milk protein result in changes of the hormonal axis of insulin, growth hormone and insulin-like growth factor-1(IGF-1) in humans. Milk consumption raises IGF-1 serum levels in the perinatal period, adolescence and adulthood. During puberty with the physiological onset of increased secretion of growth hormone, IGF-1 serum levels increase and are further enhanced by milk consumption. IGF-1 is a potent mitogen; after binding to its receptor in various tissues, it induces cell proliferation and inhibits apoptosis. Keratinocytes and sebocytes, as well as the androgen-synthesizing adrenals and gonads, are stimulated by IGF-1. The epidemic incidence of adolescent acne in Western milk-consuming societies can be explained by the increased insulin- and IGF-1-stimulation of sebaceous glands mediated by milk consumption. Acne can be regarded as a model for chronic Western diseases with pathologically increased IGF-1-stimulation. Many other organs, such as the thymus, bones, all glands, and vascular smooth muscle cells as well as neurons are subject to this abnormally increased hormonal stimulation. The milk-induced change of the IGF-1-axis most likely contributes to the development of fetal macrosomia, induction of atopy, accelerated linear growth, atherosclerosis, carcinogenesis and neurodegenerative diseases. Observations of molecular biology are supported by epidemiologic data and unmask milk consumption as a promoter of chronic diseases of Western societies.
J Dtsch Dermatol Ges 2009 Apr
PMID:Milk consumption: aggravating factor of acne and promoter of chronic diseases of Western societies. 1924 83

Psoriasis is a chronic Th-1 and Th-17 inflammatory disease. Chronic inflammation has also been associated with atherosclerosis and thrombosis. The purpose of this study was to determine the risk of stroke in patients with psoriasis. We conducted a population-based cohort study of patients seen by general practitioners participating in the General Practice Research Database in the United Kingdom, 1987-2002. Mild psoriasis was defined as any patient with a diagnostic code of psoriasis, but no history of systemic therapy. Severe psoriasis was defined as any patient with a diagnostic code of psoriasis and a history of systemic therapy consistent with severe psoriasis. The unexposed (control) population was composed of patients with no history of a psoriasis diagnostic code. When adjusting for major risk factors for stroke, both mild (hazard ratio (HR) 1.06, 95% confidence interval (CI) 1.0-1.1) and severe (1.43, 95% CI 1.1-1.9) psoriasis were independent risk factors for stroke. The excess risk of stroke attributable to psoriasis in patients with mild and severe disease was 1 in 4,115 per year and 1 in 530 per year, respectively. Patients with psoriasis, particularly if severe, have an increased risk of stroke that is not explained by major stroke risk factors identified in routine medical care.
J Invest Dermatol 2009 Oct
PMID:The risk of stroke in patients with psoriasis. 1974 78

Nicotine, one of the thousands of chemicals in cigarette smoke has a highly debated effect on cell proliferation and tissue healing. Recent studies documented its pro-angiogenesis effects by stimulating endothelial cell alpha7-non-neronal nicotinic acetyl choline receptors (alpha7 N-nACHR). It is well known that individuals who smoke or have diabetes experience impaired wound healing although for different reasons. This review evaluates several current studies relating to nicotine's ability to mediate cellular activation, migration and angiogenesis in attempts to correlate these data with nicotine's ability to repair wounds in ischaemic tissue. While its beneficial effects are still under investigation, important findings regarding nicotine's acceleration of atherosclerosis, tumor angiogenesis, cell proliferation e and resistance to apoptosis put its systemic use into question. Based on the good and bad sides of nicotine, it is recommended to restrict its utility to local applications.
Exp Dermatol 2009 Jun
PMID:The multiple faces of nicotine and its implications in tissue and wound repair. 1949 97

There is now growing evidence that psoriasis, like other inflammatory diseases such as rheumatoid arthritis and systemic lupus erythematosus, is a systemic disorder that is associated with enhanced atherosclerosis and risk of coronary artery disease. Here we summarize the available epidemiological evidence for this association and analyse pathogenic features that are common to psoriasis and atherosclerosis. Further prospective studies are urgently needed to extend knowledge of the risk of cardiovascular morbidity and mortality in patients with psoriasis and to confirm the degree to which treatment of psoriasis reduces this risk. Nevertheless, existing data are sufficient to indicate that severe psoriasis should be more widely recognized as a potential risk factor for cardiovascular disease and should be considered with the established factors when formulating strategies for the management of cardiovascular risk.
Br J Dermatol 2009 Jul
PMID:More than skin deep: atherosclerosis as a systemic manifestation of psoriasis. 1950 Jan 2

Keloids are fibrous overgrowth induced by cutaneous injury. The pathogenesis of keloids is poorly understood, and no convincing animal model exists. Current hypotheses of the pathogenesis classify keloids as an entity of aberrant fibrosis. Hyperactivation of the MCP-1/CCR2 axis reportedly causes fibrosis in liver cirrhosis, atherosclerosis and lung fibrosis. Circulating CD14+ monocytes are precursors of circulating fibrocytes and contribute to fibrogenesis by a MCP-1/CCR2-dependent loop. As there is an increase in monocyte lineages in keloids, the aim of this study is to determine whether peripheral CD14+ monocytes in keloid patients trigger fibroblast proliferation through MCP-1. Expressions of MCP-1 and its receptor CCR2 in keloid lesions were measured by immunohistochemistry and real-time PCR. The results revealed an increase in MCP-1 and CCR2 in the keloid tissues. Co-culture of keloid CD14+ cells and normal fibroblasts enhanced fibroblast proliferation and a parallel increase in extracellular MCP-1. We further found that MCP-1 modest enhanced fibroblast proliferation via Akt activation. Blockade of either MCP-1 or Akt signaling suppressed the mediation of fibroblast proliferation by CD14+ cells from patients. These results demonstrated that enhanced MCP-1 release by keloid CD14+ cells augments fibroblast proliferation via Akt pathway in keloids. We concluded that enhanced MCP-1 release by keloid CD14+ cells augments fibroblast proliferation, which might initiate keloid development.
Exp Dermatol 2010 Aug
PMID:Enhanced MCP-1 release by keloid CD14+ cells augments fibroblast proliferation: role of MCP-1 and Akt pathway in keloids. 2010 Feb

Recently, a strong association between "psoriasis" and "atherosclerosis" has emerged. Psoriasis patients have an increased prevalence of atherosclerotic disease including coronary artery, cerebrovascular, and peripheral vascular diseases. The exact connection between psoriasis and atherosclerosis remains unclear, but it is thought that inflammation, which plays an important role in both diseases, may be the causative link. Nevertheless, psoriasis patients suffer from an increased burden of atherosclerotic disease and most commonly die from "coronary artery disease" (CAD). Psoriatic patients have an increased prevalence of CAD risk factors and an increased risk of myocardial infarction (MI). One CAD risk factor in psoriasis patients that can easily be managed is "hyperlipidemia." "Statins" are safe, cost-effective, and have been proven to be highly effective in preventing CAD, including MI, in patients with hyperlipidemia. Furthermore, in addition to their lipid lowering properties, statins have anti-inflammatory immunomodulator activities that may be beneficial in several autoimmune diseases including psoriasis. Considering the safety and cost-effectiveness of statins, we feel that it is worth investigating if statins can play a dual role in psoriasis by treating the increased atherosclerotic disease burden in these patients through their lipid lowering effects and by decreasing psoriatic disease activity through their anti-inflammatory immunomodulatory properties.
Dermatol Online J 2010 Feb 15
PMID:Psoriasis: can statins play a dual role? 2017 98

We have previously postulated that as well as T-helper (Th) 1 and Th17 cells, the transforming growth factor (TGF)-beta/fibronectin (FN)/alpha5beta1 pathway is central to psoriasis pathogenesis. EDA+ FN refers to an alternatively spliced isoform of FN with an additional domain known as extra domain A. EDA+ FN has two important properties pertinent to psoriasis lesions: it stimulates keratinocyte hyperproliferation, and, through stimulation of Toll-like receptor (TLR) 4, stimulates production of proinflammatory cytokines. EDA+ FN production induced by TGF-beta stimulation can be maintained in psoriasis lesions via two main feedback loops. Firstly, EDA+ FN stimulates proliferation of keratinocytes, which, in an autocrine fashion, will release more EDA+ FN. Secondly, EDA+ FN stimulates TLR4 expressed by antigen-presenting cells resulting in the production of proinflammatory cytokines such as tumour necrosis factor-alpha, interleukin (IL)-1, IL-6 and IL-12. The resultant promotion of cutaneous inflammation results in the recruitment of Th1 cells, which also produce EDA+ FN. We propose that these 'FN loops' contribute to the maintenance and progression of psoriatic lesions. Finally, although the association between psoriasis and heart/thrombotic disease remains unclear one plausible link may be the promotion of atherosclerosis and thrombotic heart disease by EDA+ FN.
Br J Dermatol 2010 Jul
PMID:Psoriasis and extra domain A fibronectin loops. 2019 57

Hyaluronan (H) is an ubiquitous high-molecular size glycosaminoglycan involved in many physiological functions. Evidences are numerous implying H in various pathological pathways, such as inflammation, cancer cardio-vascular diseases. CD44 is the principal membrane cell receptor of H. In inflammation, H has size-specific different biological activities. The high molecular weight H are anti-angiogenic, anti-inflammatory and immunosuppressive. Smaller H oligomers are angiogenic, inflammatory and immuno-stimulatory. H is strongly involved in the recruitment of leucocytes at the site of inflammation (role of CD44). Data giving evidence for a role of H in allergic pathways and auto-immunity are scarce. H is implicated in pathogenetic process leading to atherosclerosis.
Ann Dermatol Venereol 2010 Apr
PMID:[Hyaluronan in inflammation, auto-immunity and cardio-vascular diseases]. 2043 55

Statins are competitive inhibitors of 3-hydroxy-3-methylyglutaryl-coenzyme A reductase and reduce low-density lipoprotein-C levels. Statins are well-tolerated drugs used for prevention of atherosclerosis and cardiovascular events. Statins possess anti-inflammatory, immunomodulatory, antioxidant, metabolic, and possible anticancer effects. Statins are reported to be effective against psoriasis, dermatitis, graft-versus-host disease, uremic pruritus, vitiligo, and hirsutism. Topical forms of statins are employed in the treatment of acne, seborrhea, rosacea, and rhinophyma. Animal studies show the beneficial effect of statins against contact dermatitis and wound healing. They have promising anti-HIV effects as well. This article succinctly reviews the various cellular and molecular effects of statins, their applications in cutaneous medicine and their side effects.
Int J Dermatol 2010 Nov
PMID:Statins in dermatology. 2096 47

Owing to its implication in a range of pathological conditions, including asthma, rheumatoid arthritis, atherosclerosis, inflammatory bowel disease and cancer, the pleiotropic cytokine macrophage migration inhibitory factor (MIF) has been the subject of intensive recent investigation. In the field of dermatology, MIF is believed to be a detrimental factor in diseases such as systemic sclerosis, atopic dermatitis, psoriasis, eczema and UV radiation damage. However, its contribution to other aspects of cutaneous biology is currently unclear. Although its expression in intact skin is well characterized, little is known about MIF's role in cutaneous homoeostasis. However, recent data do identify MIF as a key player in the immune privilege of hair follicles. Similarly, although MIF is rapidly released and its local expression significantly induced upon wounding, its primary role in the ensuing repair process remains a source of contention. MIF has been identified as being a key effector of the beneficial effects of estrogen on wound repair, yet studies employing Mif null mice, recombinant MIF, and neutralizing anti-MIF antibodies have failed to provide a consensus as to whether it benefits or inhibits healing. In fact MIF appears to be able to exert both positive and negative effects, with the cell-specific relevancy of MIF in wound healing still unclear. Thus, if MIF and/or its downstream targets are to be therapeutically useful in the context of cutaneous repair, more needs to be done to establish the nature and mechanism of action of MIF and its receptors in healing wounds.
Exp Dermatol 2011 Jan
PMID:MIF: a key player in cutaneous biology and wound healing. 2115 33


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