Mechanical load inhibits cancer growth in mouse and human hearts
Summary
The heart rarely develops cancer, and, at the same time, it lacks regenerative capacity, as cardiomyocytes stop proliferating after birth. This suggests that mechanisms limiting cardiac regeneration may also protect against cancer. In this work, we investigated the role of mechanical load and used in vivo cancer models and ex vivo engineered heart tissues to show that mechanical load reduces cancer cell proliferation in the myocardium. Spatial transcriptomics of human cardiac metastases re
Content
# Mechanical load inhibits cancer growth in mouse and human hearts
*Published: 2026 Apr 23*
The heart rarely develops cancer, and, at the same time, it lacks regenerative
capacity, as cardiomyocytes stop proliferating after birth. This suggests that
mechanisms limiting cardiac regeneration may also protect against cancer. In
this work, we investigated the role of mechanical load and used in vivo cancer
models and ex vivo engineered heart tissues to show that mechanical load reduces
cancer cell proliferation in the myocardium. Spatial transcriptomics of human
cardiac metastases revealed decreased histone methylation and chromatin
compaction. These changes affect chromatin accessibility at
proliferation-related loci, with Nesprin-2 identified as a key mechanosensor.
Our results uncover how mechanical forces protect the heart from cancer and
suggest potential strategies for cancer therapy based on mechanical stimulation.
DOI: 10.1126/science.ads9412