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When nature's robots go rogue: exploring protein homeostasis dysfunction and the implications for understanding human
Julie A Reisz1, Alexander S Barrett1, Travis Nemkov1
1a Department of Biochemistry and Molecular Genetics , University of Colorado Denver - Anschutz Medical Campus , Aurora , CO , USA.
Expert Review of Proteomics
|March 16, 2018
Summary
Aging and neurodegenerative diseases disrupt protein homeostasis, leading to cellular damage. Understanding these disruptions is key to developing treatments for age-related diseases and neurodegeneration.
Area of Science:
- Biochemistry
- Cell Biology
- Gerontology
Background:
- Proteins function as molecular machines essential for cellular viability.
- Protein homeostasis (proteostasis) is crucial for maintaining cellular integrity.
- Aging and neurodegenerative diseases compromise proteostasis through various mechanisms.
Purpose of the Study:
- To summarize age- and disease-related changes in proteostasis.
- To explore the interplay between aging and disease in proteostasis disruption.
- To highlight the role of proteostasis alterations in neurodegenerative diseases and other pathologies.
Main Methods:
- Review of age- and disease-related changes in protein machinery.
- Focus on proteostasis alterations in Alzheimer's, Parkinson's, Huntington's diseases, Down syndrome, ophthalmic pathologies, and cancer.
- Integration of high-throughput omics technologies and structural biochemistry approaches.
Main Results:
- Aging impairs protein repair and degradation, challenging proteostasis.
- Disruptions in proteostasis are characteristic of neurodegenerative diseases.
- Aging and disease synergistically exacerbate proteostasis damage.
Conclusions:
- Understanding proteostasis mechanisms and their dysregulation is vital for treating senescence-associated diseases.
- Advances in omics technologies and structural biochemistry are accelerating breakthroughs in proteostasis research.
- Targeting proteostasis pathways offers a promising therapeutic strategy for age-related pathologies and neurodegeneration.