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Review

Glucocorticoid-Induced Leucine Zipper (GILZ) in Cardiovascular Health and Disease

1
Department of Experimental Medicine, University of Campania ‘Luigi Vanvitelli’, 80138 Naples, Italy
2
Department of Philosophy, Social Sciences and Education, University of Perugia, 06123 Perugia, Italy
3
Department of Medical and Surgical Sciences, University ‘Magna Graecia’ of Catanzaro, 88100 Catanzaro, Italy
4
Department of Medicine and Surgery, Section of Pharmacology, University of Perugia, 06156 Perugia, Italy
5
Department of Experimental and Clinical Medicine, University ‘Magna Graecia’ of Catanzaro, 88100 Catanzaro, Italy
*
Author to whom correspondence should be addressed.
Academic Editor: Pablo García De Frutos
Cells 2021, 10(8), 2155; https://doi.org/10.3390/cells10082155
Received: 13 July 2021 / Revised: 13 August 2021 / Accepted: 16 August 2021 / Published: 21 August 2021
(This article belongs to the Special Issue Glucocorticoid-induced Proteins Annexin A1 and GILZ in Inflammation)
Glucocorticoids (GCs) are essential in regulating functions and homeostasis in many biological systems and are extensively used to treat a variety of conditions associated with immune/inflammatory processes. GCs are among the most powerful drugs for the treatment of autoimmune and inflammatory diseases, but their long-term usage is limited by severe adverse effects. For this reason, to envision new therapies devoid of typical GC side effects, research has focused on expanding the knowledge of cellular and molecular effects of GCs. GC-induced leucine zipper (GILZ) is a GC-target protein shown to mediate several actions of GCs, including inhibition of the NF-κB and MAPK pathways. GILZ expression is not restricted to immune cells, and it has been shown to play a regulatory role in many organs and tissues, including the cardiovascular system. Research on the role of GILZ on endothelial cells has demonstrated its ability to modulate the inflammatory cascade, resulting in a downregulation of cytokines, chemokines, and cellular adhesion molecules. GILZ also has the capacity to protect myocardial cells, as its deletion makes the heart, after a deleterious stimulus, more susceptible to apoptosis, immune cell infiltration, hypertrophy, and impaired function. Despite these advances, we have only just begun to appreciate the relevance of GILZ in cardiovascular homeostasis and dysfunction. This review summarizes the current understanding of the role of GILZ in modulating biological processes relevant to cardiovascular biology. View Full-Text
Keywords: glucocorticoid-induced leucine zipper; glucocorticoids; cardiovascular disease; inflammation glucocorticoid-induced leucine zipper; glucocorticoids; cardiovascular disease; inflammation
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MDPI and ACS Style

Cappetta, D.; Bereshchenko, O.; Cianflone, E.; Rossi, F.; Riccardi, C.; Torella, D.; Berrino, L.; Urbanek, K.; De Angelis, A.; Bruscoli, S. Glucocorticoid-Induced Leucine Zipper (GILZ) in Cardiovascular Health and Disease. Cells 2021, 10, 2155. https://doi.org/10.3390/cells10082155

AMA Style

Cappetta D, Bereshchenko O, Cianflone E, Rossi F, Riccardi C, Torella D, Berrino L, Urbanek K, De Angelis A, Bruscoli S. Glucocorticoid-Induced Leucine Zipper (GILZ) in Cardiovascular Health and Disease. Cells. 2021; 10(8):2155. https://doi.org/10.3390/cells10082155

Chicago/Turabian Style

Cappetta, Donato, Oxana Bereshchenko, Eleonora Cianflone, Francesco Rossi, Carlo Riccardi, Daniele Torella, Liberato Berrino, Konrad Urbanek, Antonella De Angelis, and Stefano Bruscoli. 2021. "Glucocorticoid-Induced Leucine Zipper (GILZ) in Cardiovascular Health and Disease" Cells 10, no. 8: 2155. https://doi.org/10.3390/cells10082155

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