Cellular parabiosis and the latency of age-related diseases
Cellular parabiosis is tissue-based phenotypic suppression of cellular dysfunction by intercellular molecular traffic keeping initiated age-related diseases and conditions in long latency. Interruption of cellular parabiosis (e.g. by chronic inflammation) promotes the onset of initiated pathologies....
Main Author: | |
---|---|
Format: | Article |
Language: | English |
Published: |
The Royal Society
2019-03-01
|
Series: | Open Biology |
Subjects: | |
Online Access: | https://royalsocietypublishing.org/doi/pdf/10.1098/rsob.180250 |
id |
doaj-897304acfdb74e92bc936c4a11a46b9b |
---|---|
record_format |
Article |
spelling |
doaj-897304acfdb74e92bc936c4a11a46b9b2020-11-25T03:57:03ZengThe Royal SocietyOpen Biology2046-24412019-03-019310.1098/rsob.180250180250Cellular parabiosis and the latency of age-related diseasesMiroslav RadmanCellular parabiosis is tissue-based phenotypic suppression of cellular dysfunction by intercellular molecular traffic keeping initiated age-related diseases and conditions in long latency. Interruption of cellular parabiosis (e.g. by chronic inflammation) promotes the onset of initiated pathologies. The stability of initiated latent cancers and other age-related diseases (ARD) hints to phenotypically silent genome alterations. I propose that latency in the onset of ageing and ARD is largely due to phenotypic suppression of cellular dysfunctions via molecular traffic among neighbouring cells. Intercellular trafficking ranges from the transfer of ions and metabolites (via gap junctions) to entire organelles (via tunnelling nanotubes). Any mechanism of cell-to-cell communication resulting in functional cross-complementation among the cells is called cellular parabiosis. Such ‘cellular solidarity’ creates tissue homeostasis by buffering defects and averaging cellular functions within the tissues. Chronic inflammation is known to (i) interrupt cellular parabiosis by the activity of extracellular proteases, (ii) activate dormant pathologies and (iii) shorten disease latency, as in tumour promotion and inflammaging. Variation in cellular parabiosis and protein oxidation can account for interspecies correlations between body mass, ARD latency and longevity. Now, prevention of ARD onset by phenotypic suppression, and healing by phenotypic reversion, become conceivable.https://royalsocietypublishing.org/doi/pdf/10.1098/rsob.180250cellular parabiosiscellular dysfunctionintercellular molecular traffic |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Miroslav Radman |
spellingShingle |
Miroslav Radman Cellular parabiosis and the latency of age-related diseases Open Biology cellular parabiosis cellular dysfunction intercellular molecular traffic |
author_facet |
Miroslav Radman |
author_sort |
Miroslav Radman |
title |
Cellular parabiosis and the latency of age-related diseases |
title_short |
Cellular parabiosis and the latency of age-related diseases |
title_full |
Cellular parabiosis and the latency of age-related diseases |
title_fullStr |
Cellular parabiosis and the latency of age-related diseases |
title_full_unstemmed |
Cellular parabiosis and the latency of age-related diseases |
title_sort |
cellular parabiosis and the latency of age-related diseases |
publisher |
The Royal Society |
series |
Open Biology |
issn |
2046-2441 |
publishDate |
2019-03-01 |
description |
Cellular parabiosis is tissue-based phenotypic suppression of cellular dysfunction by intercellular molecular traffic keeping initiated age-related diseases and conditions in long latency. Interruption of cellular parabiosis (e.g. by chronic inflammation) promotes the onset of initiated pathologies.
The stability of initiated latent cancers and other age-related diseases (ARD) hints to phenotypically silent genome alterations. I propose that latency in the onset of ageing and ARD is largely due to phenotypic suppression of cellular dysfunctions via molecular traffic among neighbouring cells. Intercellular trafficking ranges from the transfer of ions and metabolites (via gap junctions) to entire organelles (via tunnelling nanotubes). Any mechanism of cell-to-cell communication resulting in functional cross-complementation among the cells is called cellular parabiosis. Such ‘cellular solidarity’ creates tissue homeostasis by buffering defects and averaging cellular functions within the tissues. Chronic inflammation is known to (i) interrupt cellular parabiosis by the activity of extracellular proteases, (ii) activate dormant pathologies and (iii) shorten disease latency, as in tumour promotion and inflammaging. Variation in cellular parabiosis and protein oxidation can account for interspecies correlations between body mass, ARD latency and longevity. Now, prevention of ARD onset by phenotypic suppression, and healing by phenotypic reversion, become conceivable. |
topic |
cellular parabiosis cellular dysfunction intercellular molecular traffic |
url |
https://royalsocietypublishing.org/doi/pdf/10.1098/rsob.180250 |
work_keys_str_mv |
AT miroslavradman cellularparabiosisandthelatencyofagerelateddiseases |
_version_ |
1724462302042783744 |