Proteostasis and aging of stem cells

doi:10.1016/j.tcb.2013.09.002

Review

. 2014 Mar;24(3):161-70.

doi: 10.1016/j.tcb.2013.09.002. Epub 2013 Oct 3.

Proteostasis and aging of stem cells

David Vilchez¹, Milos S Simic², Andrew Dillin³

Affiliations

¹ Molecular and Cell Biology Department, The University of California, Berkeley, Li Ka Shing Center For Biomedical and Health Sciences, Berkeley, CA 94720, USA; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany.
² Molecular and Cell Biology Department, The University of California, Berkeley, Li Ka Shing Center For Biomedical and Health Sciences, Berkeley, CA 94720, USA; Université Pierre and Marie Curie, Paris, France.
³ Molecular and Cell Biology Department, The University of California, Berkeley, Li Ka Shing Center For Biomedical and Health Sciences, Berkeley, CA 94720, USA; Howard Hughes Medical Institute, The University of California, Berkeley, CA 94720, USA. Electronic address: dillin@berkeley.edu.

PMID: 24094931
DOI: 10.1016/j.tcb.2013.09.002

Review

Proteostasis and aging of stem cells

David Vilchez et al. Trends Cell Biol. 2014 Mar.

. 2014 Mar;24(3):161-70.

doi: 10.1016/j.tcb.2013.09.002. Epub 2013 Oct 3.

Authors

David Vilchez¹, Milos S Simic², Andrew Dillin³

Affiliations

¹ Molecular and Cell Biology Department, The University of California, Berkeley, Li Ka Shing Center For Biomedical and Health Sciences, Berkeley, CA 94720, USA; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany.
² Molecular and Cell Biology Department, The University of California, Berkeley, Li Ka Shing Center For Biomedical and Health Sciences, Berkeley, CA 94720, USA; Université Pierre and Marie Curie, Paris, France.
³ Molecular and Cell Biology Department, The University of California, Berkeley, Li Ka Shing Center For Biomedical and Health Sciences, Berkeley, CA 94720, USA; Howard Hughes Medical Institute, The University of California, Berkeley, CA 94720, USA. Electronic address: dillin@berkeley.edu.

PMID: 24094931
DOI: 10.1016/j.tcb.2013.09.002

Abstract

The accumulation of misfolded or damaged proteins is an important determinant of the aging process. Mechanisms that promote the homeostasis of the proteome, or proteostasis, can slow aging and decrease the incidence of age-related diseases. Adult stem cell function declines during the aging process of an organism. This demise of somatic stem cell function could contribute to tissue degeneration and organismal aging. Accumulation of damaged proteins in embryonic stem cells (ESCs) may also have an impact on the aging process, because the passage of these proteins to progenitor cells during asymmetric division could compromise development and aging. Therefore, proteostasis maintenance in stem cells might have an important role in organismal aging. In this review, we discuss exciting new insights into stem cell aging and proteostasis and the questions raised by these findings.

Keywords: aging; proteostasis; stem cells; stress responses.

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Proteostasis and aging of stem cells

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Proteostasis and aging of stem cells

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