This discrepancy may be attributed to the following reasons: HF-related oxidative stress and inflammation may upregulate HMGN2 expression in myocardial tissues to protect cardiomyocytes from damage; mechanical stress induced by HF may promote HMGN2-mediated actin rearrangement to adapt to changes in cardiomyocyte morphology and function, leading to its high expression in myocardial tissues. Here, HMGN2 is linked to hydrops fetalis.