Cell Hypertrophy: A Biophysical Roadblock to Reversing Kidney Injury

In anamniotes cell loss can typically be compensated for through proliferation, but in amniotes, this capacity has been significantly diminished to accommodate tissue complexity. In order to cope with the increased workload that results from cell death, instead of proliferation highly specialised post-mitotic cells undergo polyploidisation and hypertrophy. Although compensatory hypertrophy is the main strategy of repair/regeneration in various parenchymal tissues, the long-term benefits and its capacity to sustain complete recovery of the kidney has not been addressed sufficiently. In this perspective article we integrate basic principles from biophysics and biology to examine whether renal cell hypertrophy is a sustainable adaptation that can efficiently regenerate tissue mass and restore organ function, or a maladaptive detrimental response.

Automated summary

In anamniotes, cell loss can be compensated through proliferation, while in amniotes, post-mitotic cells undergo polyploidization and hypertrophy to cope with increased workload from cell death. The effectiveness of compensatory hypertrophy in sustaining complete recovery of the kidney remains insufficiently addressed.