Lipoprotein(a) and inflammation: A dangerous duet leading to endothelial loss of integrity. (May 2017)
- Record Type:
- Journal Article
- Title:
- Lipoprotein(a) and inflammation: A dangerous duet leading to endothelial loss of integrity. (May 2017)
- Main Title:
- Lipoprotein(a) and inflammation: A dangerous duet leading to endothelial loss of integrity
- Authors:
- Pirro, Matteo
Bianconi, Vanessa
Paciullo, Francesco
Mannarino, Massimo R.
Bagaglia, Francesco
Sahebkar, Amirhossein - Abstract:
- Graphical abstract: Lp(a), inflammation and endothelial injury. Abstract: Lipoprotein(a) [Lp(a)] is an enigmatic lipoprotein whose ancestral useful properties have been gradually obscured by its adverse pro-atherogenic and pro-thrombotic effects, that culminate into an increased risk of ischemic cardiovascular events. Although plasma Lp(a) levels are largely determined on a genetic basis, multiple factors have been reported to interfere with its plasma levels. Inflammation is one of these factors and it is believed to promote pro-atherogenic and pro-thrombotic changes leading to increased cardiovascular disease risk. The influence of inflammation on plasma Lp(a) levels is variable, with studies reporting either increased, reduced or unchanged Lp(a) expression and plasma concentrations following exposure to pro-inflammatory stimuli. The complex association between inflammation and Lp(a) is further amplified by additional findings showing that Lp(a) may promote the expression of a plethora of pro-inflammatory cytokines and induces the endothelium to switch into an activated status which results in adhesion molecules expression and inflammatory cells invasion into the arterial wall. In this picture, it emerges that increased plasma Lp(a) levels and inflammation may coexist and their coexistence may exert a deleterious impact on endothelial integrity both at a functional and structural level. Also, the detrimental duet of inflammation and Lp(a) may interfere with theGraphical abstract: Lp(a), inflammation and endothelial injury. Abstract: Lipoprotein(a) [Lp(a)] is an enigmatic lipoprotein whose ancestral useful properties have been gradually obscured by its adverse pro-atherogenic and pro-thrombotic effects, that culminate into an increased risk of ischemic cardiovascular events. Although plasma Lp(a) levels are largely determined on a genetic basis, multiple factors have been reported to interfere with its plasma levels. Inflammation is one of these factors and it is believed to promote pro-atherogenic and pro-thrombotic changes leading to increased cardiovascular disease risk. The influence of inflammation on plasma Lp(a) levels is variable, with studies reporting either increased, reduced or unchanged Lp(a) expression and plasma concentrations following exposure to pro-inflammatory stimuli. The complex association between inflammation and Lp(a) is further amplified by additional findings showing that Lp(a) may promote the expression of a plethora of pro-inflammatory cytokines and induces the endothelium to switch into an activated status which results in adhesion molecules expression and inflammatory cells invasion into the arterial wall. In this picture, it emerges that increased plasma Lp(a) levels and inflammation may coexist and their coexistence may exert a deleterious impact on endothelial integrity both at a functional and structural level. Also, the detrimental duet of inflammation and Lp(a) may interfere with the physiological endothelial repair response, thus further amplifying endothelial loss of integrity and protective functions. A fundamental understanding of the interaction between Lp(a) and inflammation is critical for our comprehension of the mechanisms leading to the derangement of endothelial homeostasis and vascular dysfunction. … (more)
- Is Part Of:
- Pharmacological research. Volume 119(2017:May)
- Journal:
- Pharmacological research
- Issue:
- Volume 119(2017:May)
- Issue Display:
- Volume 119 (2017)
- Year:
- 2017
- Volume:
- 119
- Issue Sort Value:
- 2017-0119-0000-0000
- Page Start:
- 178
- Page End:
- 187
- Publication Date:
- 2017-05
- Subjects:
- Lp(a) lipoprotein(a) -- LDL low-density lipoprotein -- apoB100 apolipoprotein B100 -- apo(a) apolipoprotein(a) -- CVD cardiovascular disease -- LDL-C LDL-cholesterol -- HDL-C high-density lipoprotein cholesterol -- K kringle -- PCSK9 proprotein covertase subtilisin/kexin type 9 -- OxLDL oxidized LDL -- OxPL oxidized phospholipid -- LPS lipopolysaccharide -- IAVI isolated aortic valve interstitial -- CAVD calcific aortic valve disease -- ATX autotaxin -- NF-κB nuclear factor-κB -- MCP-1 monocyte chemoattractant protein-1 -- TGF-β transforming growth factor-β -- ICAM-1 intercellular adhesion molecule-1 -- HUVEC human umbilical vein endothelial cell -- IL interleukin -- TNF-α tumour necrosis factor-α -- VCAM-1 vascular cell adhesion molecule-1 -- COX-2 cyclooxygenase-2 -- LAL lysosomal acid lipase -- CRP C-reactive protein -- VAP-1 vascular adhesion protein-1 -- MTX methotrexate -- NO nitric oxide -- EMP endothelial microparticle -- iNOS inducible nitric oxide synthase -- eNOS endothelial nitric oxide synthase -- AT1 angiotensin-1 -- Stat3 signal transducer transactivator-3 -- NADP(H) nicotinamide adenine dinucleotide phosphate -- TX thromboxane -- PGI2 prostaglandin I2 -- ADMA asymmetric dimethylarginine -- hsCRP high sensitivity CRP -- ROS reactive oxygen species -- ACh acetylcholine -- EPC endothelial progenitor cell -- VEGF-R1 vascular endothelial growth factor receptor-1 -- SDF-1 stromal cell derived factor-1 -- MLC myosin light chain -- bFGF basic fibroblast growth factor -- FMD flow-mediated dilatation
Lipoprotein(a) -- Inflammation -- Endothelial dysfunction -- Microparticles -- Progenitors
Pharmacology -- Periodicals
Pharmacology -- Periodicals
Research -- Periodicals
Médicaments -- Recherche -- Périodiques
Pharmacologie -- Périodiques
615.105 - Journal URLs:
- http://www.sciencedirect.com/science/journal/10436618 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.phrs.2017.02.001 ↗
- Languages:
- English
- ISSNs:
- 1043-6618
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 6446.550000
British Library DSC - BLDSS-3PM
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