PMID- 8699871
OWN - NLM
STAT- MEDLINE
DCOM- 19960905
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 25 Suppl 2
DP  - 1995
TI  - Cytokines regulate vascular functions related to stability of the atherosclerotic 
      plaque.
PG  - S9-12
AB  - The cytokines are multipotent mediators of inflammation and immunity that can 
      affect key functions of vascular wall cells. Growing evidence suggests that 
      cytokines participate as autocrine or paracrine mediators in atherogenesis, as 
      cells in lesions can both produce and respond to these mediators. The functions 
      of vascular wall cells regulated by cytokines may influence lesion initiation, 
      progression, or complication. For example, cytokines can regulate the expression 
      of adhesion molecules crucial to the recruitment of leukocytes to lesions, 
      including vascular cell adhesion molecule-1 (VCAM-1). Cytokines such as 
      interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) can regulate the 
      production of monocyte chemoattractant protein-1 (MCP-1), a potential signal for 
      directed migration of monocytes into the intima. Cytokines can also regulate 
      genes that encode other growth factors and cytokines themselves. TNF-alpha can 
      induce IL-1 mRNA in human endothelial (EC) and smooth-muscle cells (SMC). IL-1 
      and TNF-alpha can augment the production by vascular cells of macrophage-colony 
      stimulating factor (M-CSF), which may promote growth and activation of 
      mononuclear phagocytes. Cytokines can exert both pro-and antiatherogenic actions. 
      Activated T cells in human atheroma may secrete the lymphokine IFN-gamma, an 
      inhibitor of SMC proliferation. Cytokines influence vasomotor tone in arteries, 
      e.g., by inducing a form of nitric oxide synthase, the enzyme that synthesizes 
      the vasodilatory nitric oxide radical. The cytokines also modulate endothelial 
      functions that govern the formation and stability of blood thrombi. Finally, in 
      the late stages of the disease, matrix metalloproteinases derived from 
      macrophages or smooth-muscle cells themselves may contribute to weakening of the 
      fibrous cap in the vulnerable shoulder area, promoting plaque rupture and 
      occlusive thrombosis, culminating in the dramatic clinical manifestations of 
      atherosclerosis, including myocardial infarction and stroke. Thus, cytokines can 
      influence multiple aspects of atherogenesis and provide new and interesting 
      targets for therapeutic intervention.
FAU - Libby, P
AU  - Libby P
AD  - Department of Medicine, Brigham & Women's Hospital, Boston, Massachusetts 02115, 
      USA.
FAU - Sukhova, G
AU  - Sukhova G
FAU - Lee, R T
AU  - Lee RT
FAU - Galis, Z S
AU  - Galis ZS
LA  - eng
GR  - R01-HL34636-10/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Cytokines)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/*physiopathology
MH  - Blood Vessels/*physiopathology
MH  - Cytokines/*physiology
MH  - Extracellular Matrix/physiology
MH  - Humans
RF  - 23
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
AID - 10.1097/00005344-199500252-00003 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1995;25 Suppl 2:S9-12. doi: 
      10.1097/00005344-199500252-00003.