Leflunomide counter(akt)under-bars cardiac hypertrophy

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Author(s):	Pescatore, Luciana A. ; Laurindo, Francisco R. M. Total Authors: 2
Document type:	Journal article
Source:	Clinical Science; v. 132, n. 10, p. 5-pg., 2018-05-31.
Abstract
Cardiac hypertrophy (CH) is a major independent risk factor for heart failure and mortality. However, therapeutic interventions that target hypertrophy signaling in a load-independent way are unavailable. In a recent issue of Clinical Science (vol. 132, issue 6, 685-699), Ma et al. describe that the anti-inflammatory drug leflunomide markedly antagonized CH, dysfunction, and fibrosis induced by aortic banding or angiotensin-II in mice or by agonists in cultured cells. Unexpectedly, this occurred not via anti-inflammatory mechanisms but rather via inhibtion of Akt (protein kinase B, PKB) signaling. We further discuss the mechanisms underlying Akt activation and its effects on CH and review possible mechanisms of leflunomide effects. Despite some caveats, the availability of such a newly repurposed compound to treat CH can be a relevant advance. (AU)

FAPESP's process:	15/25923-0 - Modulation of vascular calcification by protein disulfide isomerase: study on a new transgenic mouse model
Grantee:	Luciana Pescatore Alves
Support Opportunities:	Scholarships in Brazil - Post-Doctoral


FAPESP's process:	13/07937-8 - Redoxome - Redox Processes in Biomedicine
Grantee:	Ohara Augusto
Support Opportunities:	Research Grants - Research, Innovation and Dissemination Centers - RIDC