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The important functional roles of non-protein-coding RNA have come to light since the discovery of the enzymatic activity of RNA in the mid 1980s. This Review discusses what is currently known about the role of a class of non-protein-coding RNA called microRNAs in the heart. Since the first report on this topic was published in 2005, intense research has been conducted to elucidate how microRNAs are involved in cardiovascular physiology and pathology.

Cardiomyocyte hypertrophy and apoptosis have been implicated in the loss of contractile function during heart failure (HF). Moreover, patients with HF have been shown to exhibit increased levels of tumor necrosis factor a (TNF‐a) in the myocardium. However, the multiple signal transduction pathways generating from the TNF‐α receptor in cardiomyocytes and leading preferentially to apoptosis or hypertrophy are still unknown. Here we demonstrate in neonatal rat cardiomyocytes that 1) TNF‐α induces phosphorylation of AKT, activation of NF‐κB, and the phosphorylation of JUN kinase; 2)blocking AKT activity prevents NF‐κB activation, suggesting a role for AKT in regulating NF‐κB function; 3)AKT and JUN are both critical for the hypertrophic effects of TNF‐α, since dominant‐negative mutants of these genes are capable of inhibiting TNF‐α‐induced ANF‐promoter up‐regulation and increase in cardiomyocyte cell size, and 4)blocking NF‐κB, AKT, or JUN alone or in combination does not sensitize cardiomyocytes to the proapoptotic effects of TNF‐α, in contrast to other cell types, suggesting a cardiac‐specific pathway regulating the anti‐apoptotic events induced by TNF‐α. Altogether, the data presented evidence the role of AKT and JUN in TNF‐αinduced cardiomyocyte hypertrophy and apoptosis.—Condorelli, G., Morisco, C., Latronico, M., Claudio, P. P., Dent, P., Tsichlis, P., Condorelli, G., Frati, G., Drusco, A., Croce, C. M., Napoli, C. TNF‐α signal transduction in rat neonatal cardiac myocytes: definition of pathways generating from the TNF‐α receptor. FASEB J. 16, 1732–1737 (2002)

Nitric oxide (NO) has been reported as being a key mediator of the autoimmune destruction of B-cells in type I diabetes, and studies have described a suppression of low-dose streptozotocin-induced (LDS) diabetes in mice after the use of NO synthase inhibitors. However, these studies disagree with regard to the outcome of hyperglycemia and insulitis after treatment with thesel-arginine analogs. The present study tries to clarify this topic by administeringN-nitro-l-arginine-methylester (NAME) (15 mg/d/mouse/15 d) after an LDS treatment in 108 male C57BL6/J mice.