Cardiac hypertrophy establishes itself when the heart has to pump against an increased afterload. Unlike exercise-induced hypertrophy, pathological hypertrophy is characterized by an increased amount of interstitial collagen, induction of foetal-type genes and an increased lumen size (dilatation). There is an increasing body of evidence to suggest a causative role of the p38-mitogen activated protein kinases (p38MAPKs, of which there are 4 isoforms; α, β, γ & δ) in cardiac dysfunction and progression to remodelling post-infarction or under increased afterload. The two most abundant isoforms of p38 in the heart are α and γ (1). Following aortic constriction, the γ isoform translocates into the nucleus, suggesting that the isoform may be involved in the de novo synthesis of proteins (1). It was hypothesised that inhibition/oblation of p38γMAPK would result in an altered response to pressure overload. 11 WT and 10 p38γδKO age and weight-matched mice underwent abdominal aortic banding surgery. Animals were anaesthetised using isoflurane (1.5% in 100% O2) and received post-operative analgesia (0.05mg/kg buprenorphine). Each animal had a constriction on the descending aorta using 8/0 equivalent to the diameter of a 28G needle. Cardiac function and morphometry was assessed every 14 days over a 10 week period using high resolution cardiac ultrasound (Vevo770, Visualsonics, CA). Animals were anaesthetised using isoflurane (1.5% in 100% O2). Data were analysed, using a two-way ANOVA with repeated measures with Tukey’s pairwise post-hoc test. Over the course of the experiment both cohorts showed decreased ventricle performance in response to surgery. However, at 10 weeks, left ventricle (LV) ejection fraction (EF) and fractional shortening (FS) had decreased significantly more in WT mice compared to the KO cohort (35±3 vs. 55±3% & 18±2 vs.28±2%, respectively), suggesting better preservation of cardiac function in the absence of p38γ. Similarly, ventricular mass:body mass (LVM:BM) ratio (8.3±0.8 vs. 5.8±0.2) and LV volume (77±13 vs. 41±4μl) had increased significantly in the WT mice compared to those lacking p38γ. All hearts were subjected to antibody staining, using antibodies for β-myosin heavy chain (β-MHC) at the end of the experiment. β-MHC expression had increased more in WT mice by the end of the study. This strongly suggests the involvement of p38γ (or δ) MAPK in the development of cardiac remodelling. However, little is known about the downstream pathways involved of whether inhibition of this pathway may have other, more systemic effects. In the future, we aim to determine the effects of this pathway on exercise-induced cardiac adaptation.