Abstract：
:In acute organ failure, rapid compensation of function loss assures survival. Dedifferentiation and/or proliferation of surviving parenchymal cells could imply a transient (and potentially fatal) impairment of residual functional performance. However, evolution has selected two flexible life-saving mechanisms acting synergistically on organ function recovery. Sustaining residual performance is possible when the remnant differentiated parenchymal cells avoid cell division, but increase function by undergoing hypertrophy via endoreplication, leading to polyploid cells. In addition, tissue progenitors, representing a subset of less-differentiated and/or self-renewing parenchymal cells completing cytokinesis, proliferate and differentiate to regenerate lost parenchymal cells. Here, we review the evolving evidence on polyploidization and progenitor-driven regeneration in acute liver, heart, and kidney failure with evolutionary advantages and trade-offs in organ repair.
journal_name
Trends Mol Medjournal_title
Trends in molecular medicineauthors
Lazzeri E,Angelotti ML,Conte C,Anders HJ,Romagnani Pdoi
10.1016/j.molmed.2019.02.006subject
Has Abstractpub_date
2019-05-01 00:00:00pages
366-381issue
5eissn
1471-4914issn
1471-499Xpii
S1471-4914(19)30041-3journal_volume
25pub_type
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