NF-kappaB as a molecular link between psychosocial stress and organ dysfunction.
It is well accepted that psychosocial stress contributes to the pathogenesis of hypertension, cardiovascular disease, and renal disease. Although even lay persons are aware that stress can be dangerous to health, the molecular mechanisms by which psychosocial events contribute to cellular dysfunction have hitherto been poorly understood by scientists. The pro-inflammatory transcription factor NF-kappaB has recently been identified as a potential critical bridge between stress and cellular activation. NF-kappaB activation, in turn, is known to play a pivotal role in vascular and renal disease. Activation of NF-kappaB, evoked by psychosocial stress, may directly target vessels and kidneys and thus represent an additional risk factor for cardiovascular and renal disease.
A
A
Bierhaus
P M
PM
Humpert
P P
PP
Nawroth
D000818:Animals; D002318:Cardiovascular Diseases / Q000276:immunology* / Q000503:physiopathology; D002648:Child; D006706:Homeostasis / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000276:immunology; D007674:Kidney Diseases / Q000276:immunology* / Q000503:physiopathology; D023421:Models, Animal; D016328:NF-kappa B / Q000276:immunology*; D018384:Oxidative Stress / Q000276:immunology; D013315:Stress, Psychological / Q000276:immunology* / Q000503:physiopathology
D016328:NF-kappa B