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Submaximal PPARγ activation and endothelial dysfunction: new perspectives for the management of cardiovascular disorders
TLDR
It is argued that partial/submaximal activation of PPARγ could be a major target for vascular endothelial functional improvement and the vascular protective properties of pharmacological agents, which submaximally activate PParγ, should be investigated.
Possible involvement of PPARγ-associated eNOS signaling activation in rosuvastatin-mediated prevention of nicotine-induced experimental vascular endothelial abnormalities
TLDR
Interestingly, the co-administration of peroxisome proliferator-activated receptor γ (PPARγ) antagonist, GW9662 submaximally, significantly prevented rosuvastatin-induced improvement in vascular endothelial integrity, endothelium-dependent relaxation, and nitrite/nitrate concentration in rats administered nicotine.
Perspectives in Renin-Angiotensin-Aldosterone System Blockade: What's New?
TLDR
A review discussed newly identified pharmacological interventions that interfere with overactivated RAAS and the intermediate peptides of RAAS have been identified as potential therapeutic targets to counterbalance the detrimental effects of Ang-II.