Key result
In rat cardiac myocytes, TNFR2 signaling exerted a protective role against TNFalpha-induced ROS production and cell death, acting as a critical limiting factor on predominant TNFR1 responses.
Why the study?
Does TNFalpha signaling through TNFR1 and TNFR2 alter ROS production, calcium transients, and cell survival in rat cardiac myocytes?
Population
Cardiac myocytes isolated from control rats
Comparison
TNFalpha treatment, neutralizing anti-TNFR2… vs Control (untreated or baseline)
Design
Preclinical
Authors
Loading...
TNFR2 protection in rat myocytes warrants no clinical change; hypothesis-generating for receptor balance in human HF.
Does TNFalpha signaling through TNFR1 and TNFR2 alter ROS production, calcium transients, and cell survival in rat cardiac myocytes?
The study demonstrates that TNFR2 signaling plays a protective role in cardiac myocytes, counteracting the detrimental effects of TNFR1, and suggests NAC as a tool to selectively neutralize TNFR1 effects.
Defer et al. (2007) studied Heart failure (cellular mechanisms). TNFalpha, anti-TNFR1/TNFR2 antibodies, N-acetylcysteine (NAC) vs. Control was evaluated on ROS production, [Ca(2+)] transient, cell fractional shortening, and cell survival. In rat cardiac myocytes, TNFR2 signaling exerted a protective role against TNFalpha-induced ROS production and cell death, acting as a critical limiting factor on predominant TNFR1 responses.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: