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Fausto Chiazza

Researcher at University of Turin

Publications -  54
Citations -  1715

Fausto Chiazza is an academic researcher from University of Turin. The author has contributed to research in topics: Inflammasome & Insulin resistance. The author has an hindex of 24, co-authored 53 publications receiving 1249 citations. Previous affiliations of Fausto Chiazza include University of Eastern Piedmont & Boston Children's Hospital.

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The NLRP3 Inflammasome as a novel player of the intercellular crosstalk in metabolic disorders.

TL;DR: A perspective on the current research on NLRP3 inflammasome is provided, which may represent an innovative therapeutic target to reverse the detrimental metabolic consequences of the metabolic inflammation.
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Pharmacological Inhibition of NLRP3 Inflammasome Attenuates Myocardial Ischemia/Reperfusion Injury by Activation of RISK and Mitochondrial Pathways.

TL;DR: It is demonstrated for the first time that INF4E protected against the IR-induced myocardial injury and dysfunction, by a mechanism that involves inhibition of the NLRP3 inflammasome, resulting in the activation of the prosurvival RISK pathway and improvement in mitochondrial function.
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Effects of vitamin D on insulin resistance and myosteatosis in diet-induced obese mice

TL;DR: Data indicate that vitamin D-induced selective inhibition of signaling pathways (including NF-κB, SCAP/SREBP and CML/RAGE cascades) within the skeletal muscle significantly contributed to the beneficial effects of vitamin D supplementation against diet-induced metabolic derangements.
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Acute treatment with relaxin protects the kidney against ischaemia/reperfusion injury

TL;DR: It is reported herein that rhRLX protects the kidney against I/R injury by a mechanism that involves changes in nitric oxide signalling pathway.
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Scavenging Circulating Mitochondrial DNA as a Potential Therapeutic Option for Multiple Organ Dysfunction in Trauma Hemorrhage

TL;DR: It is shown that the release of mtDNA is sufficient for the development of multiple organ injury and neutralizing mtDNA with the nucleic acid scavenging polymer, hexadimethrine bromide (HDMBr), at a clinically relevant time point in vivo would reduce the severity of organ injury in this model.