Author Correction: Myocardial reprogramming by HMGN1 underlies heart defects in trisomy 21

Nature

by Sanjeev S. Ranade

February 26, 2026

AI-Generated Deep Dive Summary

Scientists have identified a critical role of HMGN1 protein in causing heart defects associated with trisomy 21 (Down syndrome). A recent study correction clarifies that HMGN1 reprograms myocardial cells, leading to congenital heart issues. Researchers initially reported an incorrect statistical method in their analysis but have now rectified it to ensure accurate interpretation of their findings. The study revealed that HMGN1 influences gene expression during heart development, particularly in the ventricular septum. Elevated levels of HMGN1 disrupt normal cellular processes, contributing to heart malformations. The correction emphasizes that while the statistical approach was initially misstated, the overall conclusions about HMGN1's role in heart defects remain unchanged. This clarification underscores the importance of rigorous scientific reporting and transparency in research. Understanding the mechanisms behind congenital heart defects in Down syndrome could pave the way for improved clinical care and targeted therapies. The revised study highlights the significance of meticulous data analysis in advancing medical knowledge.

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Originally published on Nature on 2/26/2026