Cytokines in Atherosclerosis: Pathogenic and Regulatory Pathways

Tedgui, Alain; Mallat, Ziad

doi:10.1152/physrev.00024.2005

Cited by 1,441 publications

(1,170 citation statements)

References 792 publications

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“…20,21 IL-1b also influences the function of vessel wall elements, endothelial cells in particular and may contribute to the pathogenesis of arteriosclerosis in different ways, including by promoting coagulation and thrombosis. 22,23 Importantly, IL-1b was shown to control tumor angiogenesis and invasiveness of different tumor cells in mice. 24,25 Moreover, IL-1b plays a role in destructive joint and bone diseases.…”

Section: Caspase-1 and It Substrate Il-1bmentioning

confidence: 99%

Inflammatory caspases and inflammasomes: master switches of inflammation

2006

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Fifteen years have passed since the cloning and characterization of the interleukin-1b-converting enzyme (ICE/caspase-1), the first identified member of a family of proteases currently known as caspases. Caspase-1 is the prototypical member of a subclass of caspases involved in cytokine maturation termed inflammatory caspases that also include caspase-4 caspase -5, caspase -11 and caspase -12. Efforts to elucidate the molecular mechanisms involved in the activation of these proteases have uncovered an important role for the NLR family members, NALPs, NAIP and IPAF. These proteins promote the assembly of multiprotein complexes termed inflammasomes, which are required for activation of inflammatory caspases. This article will review some evolutionary aspects, biochemical evidences and genetic studies, underlining the role of inflammasomes and inflammatory caspases in innate immunity against pathogens, autoinflammatory syndromes and in the biology of reproduction. Inflammatory CaspasesThe history of caspases began with the identification of an aspartate-specific protease activity involved in the conversion of the 31 kDa proIL-1b precursor to its active 17 kDa biologically active form, 1,2 and the identification of caspase-1 as the protease responsible for proIL-1b maturation. 3,4 The subsequent discovery of ced-3, that shares similarities with caspase-1 and which is involved in programmed cell death (PCD) in Caenorhabditis elegans, suggested that caspases might play fundamental roles in apoptosis. 5 As reviewed in the papers accompanying this issue of Cell Death and Differentiation, the role of apoptotic caspases in C. elegans and in vertebrates is crucial and deal with many facets of cell biology, development and diseases. In this review, we will focus on a subset of caspases present only in vertebrates and known as inflammatory caspases.Inflammatory caspases (also known as group I caspases) are encoded by three main genes in humans caspase-1, caspase-4 and caspase-5 and three main genes in mouse, caspase-1, caspase-11 and caspase-12. 6,7 In mammals, these caspases are characterized by the presence of a CARD domain at the N-terminus (Figure 1a). Human, chimp and mouse inflammatory caspases share significant similarity and are organized in a single locus (Figure 1c). Phylogenetic analysis of the conserved CARD domain suggests that the inflammatory caspases can be separated in evolutionaryrelated clusters (Figure 1b). The caspase-1 cluster contains caspase-1 and four other genes encoding decoy caspases: cop, inca1, inca2 and iceberg. These decoy caspase-1-like genes are absent in the mouse genome, suggesting that they have arisen recently by duplication of caspase-1. Although human and mouse caspase-1 are likely orthologues, sequence analysis suggests that human caspase-4 and caspase-5 have originated from a duplication of caspase-11. 7 However, the human caspase-12 gene, which in the chimp genome contains an SHG box important for it enzymatic activity, 8 evolved towards an enzymatically inactive form at some stage...

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Section: Caspase-1 and It Substrate Il-1bmentioning

confidence: 99%

Inflammatory caspases and inflammasomes: master switches of inflammation

2006

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“…In atherosclerosis, the activation of ECs in response to an inflammatory state leads to the expression and release of cytokines and chemokines, specifically interleukin (IL)-6 and monocyte chemoattractant protein (MCP)-1. These have been suggested to play the key role in the initial phase of atherosclerosis [20][21][22]. An increase in IL-6 levels has been associated with an increase in cardiovascular mortality in HIV-infected individuals [20], and MCP-1 has been shown to play a part in the attraction, migration, and activation of monocytes [23].…”

Section: Pathophysiology Of Coronary Artery Disease In Patients With mentioning

confidence: 99%

Coronary Artery Disease in Patients with HIV Infection

Patel

Budoff

2015

Am J Cardiovasc Drugs

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“…Les travaux chez l'animal et chez l'homme ont clairement montré que l'athérosclérose est une maladie inflammatoire chronique de la paroi des artères de gros et moyen calibre [3,4,37]. Les différentes étapes de l'athérogenèse comprennent la rétention et la modification oxydative des lipoprotéines dans l'espace sous-endothélial, l'activation et le dysfonctionnement des cellules endothéliales, puis l'adhésion, la migration et l'activation des leucocytes dans la paroi vasculaire.…”

Section: Physiopathologie De L'athérosclérose Et Phospolipases A2unclassified