ReviewInternational journal of cell biology2013
Role of protein misfolding and proteostasis deficiency in protein misfolding diseases and aging.
Review in International journal of cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 127 citations in OpenAlex.
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- Proteasome Subunits Regulate Reproduction inInsects · 2025Article
- Achieving High Protein Quality Is a Challenge in Vegan Diets: A Narrative Review.Nutrition reviews · 2025Review
- Targeting aging hallmarks in brain health within the framework of preventive medicine: mechanistic insights into naringenin's role in longevity, synaptic function, and cellular homeostasis.Frontiers in nutrition · 2025Review
- From Molecular to Radionuclide and Pharmacological Aspects in Transthyretin Cardiac Amyloidosis.International journal of molecular sciences · 2024Review
- Mitochondrial Dysfunction and Protein Homeostasis in Aging: Insights from a Premature-Aging Mouse Model.Biomolecules · 2024Article
- Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.Physiological reviews · 2024Review
- Transcriptomic analyses reveal proinflammatory activation of human brain microvascular endothelial cells by aging-associated peptide medin and reversal by nanoliposomes.Scientific reports · 2023Article
- Mitochondrial and Proteasome Dysfunction Occurs in the Hearts of Mice Treated with Triazine Herbicide Prometryn.International journal of molecular sciences · 2023Article
- Morphometric and Nanomechanical Screening of Peripheral Blood Cells with Atomic Force Microscopy for Label-Free Assessment of Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- Challenges and limitations in computational prediction of protein misfolding in neurodegenerative diseases.Frontiers in computational neuroscience · 2023Article
- LRRK2 and Proteostasis in Parkinson's Disease.International journal of molecular sciences · 2022Review
- Contiguously hydrophobic sequences are functionally significant throughout the human exome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Extensive accumulation of misfolded protein aggregates during natural aging and senescence.Frontiers in aging neuroscience · 2022Article
- Roles and Mechanisms of the Protein Quality Control System in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Singular value decomposition analysis of the secondary structure features contributing to the circular dichroism spectra of model proteins.Biochemistry and biophysics reports · 2021Article
- mTOR in Alzheimer disease and its earlier stages: Links to oxidative damage in the progression of this dementing disorder.Free radical biology & medicine · 2021Review
- The Ubiquitin Proteasome System in Neuromuscular Disorders: Moving Beyond Movement.International journal of molecular sciences · 2020Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The misfolding, aggregation, and tissue accumulation of proteins are common events in diverse chronic diseases, known as protein misfolding disorders. Many of these diseases are associated with aging, but the mechanism for this connection is unknown. Recent evidence has shown that the formation and accumulation of protein aggregates may be a process frequently occurring during normal aging, but it is unknown whether protein misfolding is a cause or a consequence of aging. To combat the formation of these misfolded aggregates cells have developed complex and complementary pathways aiming to maintain protein homeostasis. These protective pathways include the unfolded protein response, the ubiquitin proteasome system, autophagy, and the encapsulation of damaged proteins in aggresomes. In this paper we review the current knowledge on the role of protein misfolding in disease and aging as well as the implication of deficiencies in the proteostasis cellular pathways in these processes. It is likely that further understanding of the mechanisms involved in protein misfolding and the natural defense pathways may lead to novel strategies for treatment of age-dependent protein misfolding disorders and perhaps aging itself.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.