PMID- 26702404
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2305-6304 (Print)
IS  - 2305-6304 (Electronic)
IS  - 2305-6304 (Linking)
VI  - 3
IP  - 4
DP  - 2015
TI  - Oxyradical Stress, Endocannabinoids, and Atherosclerosis.
PG  - 481-498
AB  - Atherosclerosis is responsible for most cardiovascular disease (CVD) and is 
      caused by several factors including hypertension, hypercholesterolemia, and 
      chronic inflammation. Oxidants and electrophiles have roles in the 
      pathophysiology of atherosclerosis and the concentrations of these reactive 
      molecules are an important factor in disease initiation and progression. 
      Overactive NADPH oxidase (Nox) produces excess superoxide resulting in oxidized 
      macromolecules, which is an important factor in atherogenesis. Although 
      superoxide and reactive oxygen species (ROS) have obvious toxic properties, they 
      also have fundamental roles in signaling pathways that enable cells to adapt to 
      stress. In addition to inflammation and ROS, the endocannabinoid system (eCB) is 
      also important in atherogenesis. Linkages have been postulated between the eCB 
      system, Nox, oxidative stress, and atherosclerosis. For instance, CB(2) 
      receptor-evoked signaling has been shown to upregulate anti-inflammatory and 
      anti-oxidative pathways, whereas CB(1) signaling appears to induce opposite 
      effects. The second messenger lipid molecule diacylglycerol is implicated in the 
      regulation of Nox activity and diacylglycerol lipase beta (DAGLbeta) is a key 
      biosynthetic enzyme in the biosynthesis eCB ligand 2-arachidonylglycerol (2-AG). 
      Furthermore, Nrf2 is a vital transcription factor that protects against the 
      cytotoxic effects of both oxidant and electrophile stress. This review will 
      highlight the role of reactive oxygen species (ROS) in intracellular signaling 
      and the impact of deregulated ROS-mediated signaling in atherogenesis. In 
      addition, there is also emerging knowledge that the eCB system has an important 
      role in atherogenesis. We will attempt to integrate oxidative stress and the eCB 
      system into a conceptual framework that provides insights into this pathology.
FAU - Matthews, Anberitha T
AU  - Matthews AT
AD  - Center for Environmental Health Sciences, Department of Basic Sciences, College 
      of Veterinary Medicine, Mississippi State University, P.O. Box 6100, Mississippi 
      State, MS 39762, USA.
FAU - Ross, Matthew K
AU  - Ross MK
AD  - Center for Environmental Health Sciences, Department of Basic Sciences, College 
      of Veterinary Medicine, Mississippi State University, P.O. Box 6100, Mississippi 
      State, MS 39762, USA.
LA  - eng
GR  - F31 HL122082/HL/NHLBI NIH HHS/United States
GR  - R15 ES015348/ES/NIEHS NIH HHS/United States
PT  - Journal Article
DEP - 20151203
PL  - Switzerland
TA  - Toxics
JT  - Toxics
JID - 101639637
PMC - PMC4686160
MID - NIHMS742498
OTO - NOTNLM
OT  - 2-arachidonoylglycerol
OT  - NADPH oxidase
OT  - anandamide
OT  - atherogenesis
OT  - cardiovascular disease
OT  - reactive oxygen species
COIS- The authors declare no conflict of interest.
EDAT- 2015/12/25 06:00
MHDA- 2015/12/25 06:01
PMCR- 2015/12/03
CRDT- 2015/12/25 06:00
PHST- 2015/12/25 06:00 [entrez]
PHST- 2015/12/25 06:00 [pubmed]
PHST- 2015/12/25 06:01 [medline]
PHST- 2015/12/03 00:00 [pmc-release]
AID - toxics-03-00481 [pii]
AID - 10.3390/toxics3040481 [doi]
PST - ppublish
SO  - Toxics. 2015;3(4):481-498. doi: 10.3390/toxics3040481. Epub 2015 Dec 3.