The paper entitled "Identification of a New Modulator of the Intercalated Disc in a Zebrafish Model of Arrhythmogenic Cardiomyopathy", as published in 2014 in Science Translational Medicine, examined the effects of the newly discovered drug SB216763 (SB21) on arrhythmogenic cardiomyopathy (ACM). In this paper, the authors focused on mechanisms underlying ACM and the accompanying molecular and cellular alterations. Most importantly they showed that SB21 was able to rescue and partly reverse the ACM phenotype in three different experimental models: (I) a zebrafish model of Naxos disease induced by the overexpression of the 2057del2 mutation in plakoglobin (PKG); (II) neonatal rat cardiomyocytes overexpressing the same mutation in PKG; (III) cardiomyocytes derived from induced pluripotent stem cells expressing two different forms of mutations in plakophilin-2. This editorial will focus on the potency and possible restrictions concerning SB21 treatment as a potential intervention for ACM and the usefulness of the applied zebrafish models in general.

01 Oct 2014·Journal of HepatologyQ1 · MEDICINE

Inhibition of glycogen synthase kinase 3 ameliorates liver ischemia/reperfusion injury via an energy-dependent mitochondrial mechanism

Q1 · MEDICINE

Article

Author: Zhang, Qingqing ; Miao, Mingyong ; Shi, Xueyin ; Xu, Haitao ; Chen, Huan ; Zhu, Qiufeng ; Li, Yonghua ; Yuan, Hongbin ; Li, Weiwei ; Liu, Fang ; Fu, Hailong ; Wang, Quanxing

BACKGROUND & AIMSThe mechanisms of glycogen synthase kinase-3 (GSK-3)-mediated cytoprotection during liver ischemia/reperfusion (I/R) remain controversial, particularly in older organs. This study explores the role and potential mechanisms of GSK-3 in young and aging livers.METHODSA rodent partial warm I/R model was used to evaluate the therapeutic potential of GSK-3 modulation during hepatic I/R in young and aging Sprague-Dawley rats.RESULTSGSK-3 inhibition through IPC or SB216763 (SB21) preconditioning protected young rats from I/R-induced liver injury. This protection was absent in old animals but could be restored by glucose infusion prior to the I/R insult. The protection conferred by GSK-3 inhibition depended on mitochondrial metabolism regulation. Indeed, the inhibition of GSK-3 suppressed mitochondrial permeability transition pore (MPTP) opening, triggering mitohormesis in young animals, whereas insufficient fuel suppressed mitochondrial metabolism and inactivated the GSK-3-related protection in old animals. SB21 and glucose reactivated the mitochondrial F0F1-ATPase and subsequent protective cascades in the senescent liver. These effects were antagonized by an ATPase inhibitor and by an MPTP opener.CONCLUSIONSThe protection conferred by GSK-3 inhibition during hepatic I/R insult is energy dependent, particularly in senescent livers. These findings demonstrate a key role for GSK-3-related mitochondrial energy homeostasis, which may shed new light on the clinical use of GSK-3 inhibitors to protect liver function in surgical settings, particularly for older patients.

15 Oct 2008·Applied and Environmental MicrobiologyQ2 · BIOLOGY

Identification of Critical Members in a Sulfidogenic Benzene-Degrading Consortium by DNA Stable Isotope Probing

Q2 · BIOLOGY

Article

Author: Phelps, C. D. ; McGuinness, L. M. ; Oka, A. R. ; Mumford, A. ; Young, L. Y. ; Kerkhof, L. J.

ABSTRACT Stable isotope probing (SIP) was used to identify the active members in a benzene-degrading sulfidogenic consortium. SIP-terminal restriction fragment length polymorphism analysis indicated that a 270-bp peak incorporated the majority of the 13 C label and is a sequence closely related to that of clone SB-21 (GenBank accession no. AF029045). This target may be an important biomarker for anaerobic benzene degradation in the field.

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Indication	Highest Phase	Country/Location	Organization	Date
Pulmonary Disease, Chronic Obstructive	Discovery	DE	sterna biologicals GmbH	-

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