Format

Send to

Choose Destination
Trends Mol Med. 2019 Mar 26. pii: S1471-4914(19)30041-3. doi: 10.1016/j.molmed.2019.02.006. [Epub ahead of print]

Surviving Acute Organ Failure: Cell Polyploidization and Progenitor Proliferation.

Author information

1
Department of Biological and Experimental Medical Science 'Mario Serio', Excellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE).
2
Medizinische Klinik und Poliklinik IV, Klinikum der LMU München, Munich, Germany.
3
Department of Biological and Experimental Medical Science 'Mario Serio', Excellence Centre for Research, Transfer and High Education for the Development of DE NOVO Therapies (DENOTHE); Meyer Children's Hospital, Florence, Italy. Electronic address: http://www.twitter.com/PRomagnani.

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.

KEYWORDS:

acute injury; endocycle; hypertrophy; mitosis; multinuclear; recovery

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center