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  • br Conclusions Drosophila melanogaster has increased


    Conclusions Drosophila melanogaster has increased our understanding of the molecular bases of cardiac aging over recent decades. During which, the tools available for investigating the gene 186689-07-6 patterns and physiological changes involved, have advanced considerably. In humans, cardiac aging studies are frequently limited to analysis of heart performance, genomic testing, and family history records. While these are highly valuable for understanding genetic and phenotypic trends in cardiac function over time, the ability to non-invasively investigate acute transcriptomic and proteomic changes in human tissue is impossible. Cardiac senescence is a complex event, and evidence supporting the use of Drosophila melanogaster to examine various facets of it that are difficult to study in humans grows each year. It is clear from the information presented here that multiple conserved changes inside the cell and in the ECM contribute to the overall decline in heart function over time, and there is not likely a single molecular target that will reverse this deterioration (Fig. 3). Thus, the molecular mechanisms behind the physiological changes of the aging heart must be studied further, and the Drosophila model with its limited redundancy of conserved pathways continues to be valuable for such studies. Moreover, the fly is ideally suited for probing epigenetic plasticity and drift since environmental cues can be tightly controlled and the genetics and epigenetics precisely manipulated. Overall, understanding the mechanisms behind known physiological and molecular hallmarks of cardiac aging is essential to improving heart health in our aging populations.
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    Introduction The cardiac wound healing process after myocardial infarction (MI) is divided into three distinct, but temporally overlapping, phases of infarct healing: an inflammatory phase, a proliferative phase, and a maturation phase [1]. Optimal healing of the left ventricle (LV) requires mechanisms to initiate an inflammatory response, mechanisms to resolve inflammation by inhibiting pro-inflammatory cytokines and clearing inflammatory cells, and mechanisms to induce repair [[2], [3], [4], [5], [6]]. Markers of inflammation, including myeloperoxidase (MPO) and white blood cell count (WBC), are strong predictors of post-MI adverse remodeling [[7], [8], [9]]. When WBC was used as a marker for post-MI in-hospital mortality, the pattern followed a J curve shape [10]. Patients with <1.0 × 103 cell/mL WBC had a mortality rate of 29%, which decreased to 4% in patients with 5–6 × 103/mL WBC. When WBC increased to over 25 × 103/mL, mortality increased to 35% indicating that too few or too many inflammatory cells adversely affected the post-MI wound healing response. Better biomarkers are needed to improve diagnosis, guide molecular target therapy, and monitor activity and therapeutic response in post-MI patients. An ideal biomarker has the following characteristics: high specificity, sensitivity, accessibility, speed, and cost-effectiveness [11]. Recent advances in genomic and proteomic approaches have increased the number of diagnostic marker candidates [12]. The Mississippi Center for Heart Research developed the Mouse Heart Attack Research Tool (mHART) as a means to consolidate results into an easily searchable format to facilitate broad use of big data analysis [13]. Because LV dilation is a strong predictor of post-MI survival [14], the goal of this study was to identify biomarkers that linked to the post-MI LV dilation phenotype. We hypothesized that using the mHART database would allow us to isolate the molecular and cellular LV dilation phenotype.
    Materials and methods
    Discussion This is the first report that has assigned a positive role for MIP-1γ in post-MI wound healing. MIP-1γ/Ccl9 is a chemotactic protein secreted by neutrophils and macrophages that regulates the wound healing response in multiple disease processes, including cutaneous wound healing [[31], [32], [33], [34]]. MIP-1γ inhibition reduces neutrophil and macrophage infiltration, collagen deposition, and improves pulmonary function in a mouse model of chronic graft-versus-host disease [33]. MIP-1γ has been shown to correlate with the extent of atherosclerotic lesions [35]. While not previously evaluated in the MI setting, a similar inhibition phenotype would be detrimental for MI remodeling. In addition, in a model of colon cancer, MIP-1γ promotes recruitment of the matrix metalloproteinase-expressing stromal cells [32], consistent with a positive role in necrotic tissue removal.