Key result
Telmisartan delays endothelial cell senescence and increases nitric oxide synthesis by activating PPARgamma signaling.
Why the study?
Does telmisartan delay senescence and alter the ADMA-DDAH-NO system in endothelial cells?
Population
Endothelial cells (ECs) cultured until the twelfth passage
Comparison
Telmisartan vs Eprosartan, Ang II, GW9662, and PPARgamma…
Design
Preclinical
Follow-up
until the twelfth passage
Authors
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Hypothesis-generating for telmisartan in endothelial senescence; human trials needed to confirm PPARgamma-DDAH effects.
Does telmisartan delay senescence and alter the ADMA-DDAH-NO system in endothelial cells?
Telmisartan delays endothelial senescence through PPARgamma-mediated upregulation of DDAH, leading to decreased ADMA and increased NO synthesis.
Scalera et al. (2008) studied Endothelial cell aging. Telmisartan vs. Eprosartan, Ang II, and GW9662 was evaluated on Nitric oxide synthesis, ADMA concentration, and cellular senescence. Telmisartan delayed endothelial cell senescence and increased nitric oxide synthesis by activating PPARgamma signaling, which upregulated DDAH expression and decreased ADMA concentration.
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