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Aim: The aim was to carry out a preliminary investigation to identify new biomarkers and test the suitability of the pro-inflammatory nuclear protein, HMGB1, as a potential diagnostic or treatment target for DCM. Background: . This study investigates whether HMGB1 is capable of attenuating the inflammation that manifests from DCM in pre-clinical models of mouse and rat combined. Methodology: A systematic review and a meta-analysis were performed by searching 5 electronic databases and retrieving 2979 articles from which 29 qualified as included studies for reporting 37 biomarkers that were grouped into 8 preclinical DCM biomarker models. The standardized mean difference (SMD or the effect size), non-parametric Mann Whitney U test, ROC, correlation coefficient and coefficient of determination were carried out in this evaluation. Results: 28 heterogeneous proinflammatory biomarkers were identified as carrying a significantly high risk of developing DCM out of the total of 37 biomarkers evaluated in forest plots in which, the highest SMD was produced by cardiac troponin (CTPN). 8 significantly high biomarkers (HMGB1, HW/BW, EF%, FS%, BG, TC, TG, NF-kB) were identified out of 37 in the non-parametric Mann Whitney U test in the DCM group compared to the HC. The correlation coefficient between HMGB1 as the independent variable produced a significant negative (ecological) correlation with HR, EF% and TLR4 at p < 0.05. Conclusion: The ability of HMGB1 in downregulating inflammation or the direct inhibition of HMGB1 using small molecules or blocking of HMGB1/TLR4/NF-kB signalling pathway could be a novel potential mechanism to resolving DCM which requires further investigations. Systematic review registration: https://www.crd.york.ac.uk/prospero/, identifier CRD42024597641.
Ranasinghe et al. (Wed,) studied this question.
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