Sean P. Barry

TL;DR: It is demonstrated that mice deficient in MKP-1 attenuates the activities of p38 MAPK and JNK to regulate both pro- and anti-inflammatory cytokines in TLR signaling, which highlights the complex mechanisms by which the MAPKs regulate innate immunity.

TL;DR: The various molecular pathways responsible for the co-ordinated control of the hypertrophic program including: natriuretic peptides, the adrenergic system, adhesion and cytoskeletal proteins, IL-6 cytokine family, MEK-ERK1/2 signalling, histone acetylation, calcium-mediated modulation and the exciting recent discovery of the role of microRNAs in controlling cardiac hypertrophy are discussed.

TL;DR: Recent advances in the understanding of how the JAK-STAT pathway orchestrates the response to cellular damage in the myocardium are discussed, along with the potential benefits and challenges in manipulating this pathway in cardiovascular therapy.

TL;DR: It is shown that cells lacking STAT3 are less efficient in repairing damaged DNA and that MDC1, a regulator of the ATM‐Chk2 pathway and facilitator of the DNA damage response, is modulated by STAT3 at the transcriptional level.

TL;DR: The molecular changes which occur in the heart in response to increased load and the pathways which control cardiac hypertrophy, calcium homeostasis, and immune activation during HF are reviewed and the newly emerging roles of microRNAs in regulating left ventricular dysfunction and fibrosis are discussed.