Cell size control – a mechanism for maintaining fitness and function
(2017) In BioEssays 39(9).- Abstract
The maintenance of cell size homeostasis has been studied for years in different cellular systems. With the focus on ‘what regulates cell size’, the question ‘why cell size needs to be maintained’ has been largely overlooked. Recent evidence indicates that animal cells exhibit nonlinear cell size dependent growth rates and mitochondrial metabolism, which are maximal in intermediate sized cells within each cell population. Increases in intracellular distances and changes in the relative cell surface area impose biophysical limitations on cells, which can explain why growth and metabolic rates are maximal in a specific cell size range. Consistently, aberrant increases in cell size, for example through polyploidy, are typically... (More)
The maintenance of cell size homeostasis has been studied for years in different cellular systems. With the focus on ‘what regulates cell size’, the question ‘why cell size needs to be maintained’ has been largely overlooked. Recent evidence indicates that animal cells exhibit nonlinear cell size dependent growth rates and mitochondrial metabolism, which are maximal in intermediate sized cells within each cell population. Increases in intracellular distances and changes in the relative cell surface area impose biophysical limitations on cells, which can explain why growth and metabolic rates are maximal in a specific cell size range. Consistently, aberrant increases in cell size, for example through polyploidy, are typically disadvantageous to cellular metabolism, fitness and functionality. Accordingly, cellular hypertrophy can potentially predispose to or worsen metabolic diseases. We propose that cell size control may have emerged as a guardian of cellular fitness and metabolic activity.
(Less)
- author
- Miettinen, Teemu P.
; Caldez, Matias J.
; Kaldis, Philipp
LU
and Björklund, Mikael
- publishing date
- 2017-09
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- cell size control, fitness, metabolism, mevalonate pathway, mitochondria, polyploidy, statin
- in
- BioEssays
- volume
- 39
- issue
- 9
- article number
- 1700058
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- scopus:85026430693
- pmid:28752618
- ISSN
- 0265-9247
- DOI
- 10.1002/bies.201700058
- language
- English
- LU publication?
- no
- id
- 85402cdf-6fec-47a6-abb7-48725160e33c
- date added to LUP
- 2019-09-18 10:14:10
- date last changed
- 2024-04-16 20:54:40
@article{85402cdf-6fec-47a6-abb7-48725160e33c, abstract = {{<p>The maintenance of cell size homeostasis has been studied for years in different cellular systems. With the focus on ‘what regulates cell size’, the question ‘why cell size needs to be maintained’ has been largely overlooked. Recent evidence indicates that animal cells exhibit nonlinear cell size dependent growth rates and mitochondrial metabolism, which are maximal in intermediate sized cells within each cell population. Increases in intracellular distances and changes in the relative cell surface area impose biophysical limitations on cells, which can explain why growth and metabolic rates are maximal in a specific cell size range. Consistently, aberrant increases in cell size, for example through polyploidy, are typically disadvantageous to cellular metabolism, fitness and functionality. Accordingly, cellular hypertrophy can potentially predispose to or worsen metabolic diseases. We propose that cell size control may have emerged as a guardian of cellular fitness and metabolic activity.</p>}}, author = {{Miettinen, Teemu P. and Caldez, Matias J. and Kaldis, Philipp and Björklund, Mikael}}, issn = {{0265-9247}}, keywords = {{cell size control; fitness; metabolism; mevalonate pathway; mitochondria; polyploidy; statin}}, language = {{eng}}, number = {{9}}, publisher = {{John Wiley & Sons Inc.}}, series = {{BioEssays}}, title = {{Cell size control – a mechanism for maintaining fitness and function}}, url = {{http://dx.doi.org/10.1002/bies.201700058}}, doi = {{10.1002/bies.201700058}}, volume = {{39}}, year = {{2017}}, }