Tumour necrosis factor-alpha (TNFα) acts as a mediator of both pathogenic inflammatory pathways and adaptive cardiac cell survival, growth, and differentiation in response to biomechanical stress.
Time for primary review 21 days. Tumour necrosis factor-alpha (TNFα) is a multifunctional cytokine that has been implicated as mediator of diverse physiologic and pathophysiologic events. These processes include inflammation, cellular survival, growth, differentiation and apoptosis. The local homeostatic cellular effects of cytokines may be considered ‘autocoid’ in nature. This word is derived from the Greek words autos (‘self’) and akos (‘remedy’), and refers to locally acting, biologically active agents, both peptides and non-peptides, that are distinct from neurotransmitters and hormones 1. Recent studies have highlighted the pathogenic role of TNFα in the development of myocardial disease, such as the direct correlation between serum TNFα levels and the severity and progression of heart failure 2–4 and the development of myocarditis in mice that overexpress TNFα specifically in the heart 5. Taken together, these studies suggest that TNFα is a mediator of cardiac pathology, acting at least in part via inflammatory pathways and via the activation of programmed cell death i. e. apoptosis 6, 7. However, in addition to mediating inflammation and apoptosis, cytokines play a critical role in the control and maintenance of signalling pathways that regulate mammalian physiology in multiple organ systems. Specifically in the heart, biomechanical stress promotes endogenous TNFα production by myocytes and non-myocytes. Therefore, as in other organ systems, the question arising is whether TNFα plays an adaptive role in mediating cardiac cell growth and in remodelling the cardiac extracellular matrix in response to biomechanical stress. The hypothesis that TNFα could have a short term adaptive and long term maladaptive role was proposed and reviewed by Mann 8 in 1996. Recent studies support the view that TNFα can have beneficial effects in cardiac homeostasis. In this mini-review we will focus on the role of TNFα in mediating myocardial cell survival, growth and differentiation as adaptation … * Corresponding author. Tel.: +27-21-406-6358; fax: +27-21-447-8789 sackatsamiot. uct. ac. za
M. Sack (Tue,) conducted a review in Myocardial hypertrophy and ischaemia. Tumour necrosis factor-alpha (TNFα) was evaluated. Tumour necrosis factor-alpha (TNFα) acts as a mediator of both pathogenic inflammatory pathways and adaptive cardiac cell survival, growth, and differentiation in response to biomechanical stress.