Zélia Gouveia

TL;DR: Targeting “free heme” may be used as a therapeutic intervention against diseases related to oxidative stress and immune-mediated inflammatory conditions.

TL;DR: It is demonstrated that the establishment of disease tolerance to malaria relies on a tissue damage-control mechanism that operates specifically in renal proximal tubule epithelial cells (RPTEC), which relies on the induction of heme oxygenase-1 and ferritin H chain via a mechanism that involves the transcription-factor nuclear-factor E2-related factor-2 (NRF2).

TL;DR: A panel of heme‐specific single domain antibodies (sdAbs) that neutralize the pro‐oxidant activity of soluble heme in vitro are developed and characterized, suggesting that these maybe used to counter the pathologic effects of labile heme during hemolytic conditions.

TL;DR: Experimental evidence is provided that heme increases portal pressure via a mechanism that involves hepatic stellate cell-mediated sinusoidal constriction, a hallmark of microcirculatory failure under stress conditions and it is proposed that he me scavenging might be used therapeutically to maintain hepatic microcirculation and organ function in sepsis.

TL;DR: Spectroscopic data and MD calculations revealed subtle differences in the binding properties and structural features of formed CO and NO adducts, but also indicated a possibility that a (5c) high-spin/(6c) low-spin redox-linked equilibrium could drive the physiological sensing of Gs cells.