Cited by 390Mitochondrial Function and PathologyAutophagy in Disease and TherapyGenetics, Aging, and Longevity in Model Organisms

Cell biology of the mitochondrion

Open access
van der Bliek, Alexander M, Sedensky, Margaret M, Morgan, Phil G·2017·Genetics

Abstract

Mitochondria are best known for harboring pathways involved in ATP synthesis through the tricarboxylic acid cycle and oxidative phosphorylation. Major advances in understanding these roles were made with Caenorhabditiselegans mutants affecting key components of the metabolic pathways. These mutants have not only helped elucidate some of the intricacies of metabolism pathways, but they have also served as jumping off points for pharmacology, toxicology, and aging studies. The field of mitochondria research has also undergone a renaissance, with the increased appreciation of the role of mitochondria in cell processes other than energy production. Here, we focus on discoveries that were made using C. elegans, with a few excursions into areas that were studied more thoroughly in other organisms, like mitochondrial protein import in yeast. Advances in mitochondrial biogenesis and membrane dynamics were made through the discoveries of novel functions in mitochondrial fission and fusion proteins. Some of these functions were only apparent through the use of diverse model systems, such as C. elegans. Studies of stress responses, exemplified by mitophagy and the mitochondrial unfolded protein response, have also benefitted greatly from the use of model organisms. Recent developments include the discoveries in C. elegans of cell autonomous and nonautonomous pathways controlling the mitochondrial unfolded protein response, as well as mechanisms for degradation of paternal mitochondria after fertilization. The evolutionary conservation of many, if not all, of these pathways ensures that results obtained with C. elegans are equally applicable to studies of human mitochondria in health and disease.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1534/genetics.117.300262

Cites

232 of 232 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Mitochondria are the principal source of ATP, which is formed by oxidative phosphorylation following electron flow through highly integrated protein complexes.

    “Mitochondria are the principal source of ATP, which is formed by oxidative phosphorylation following electron flow through highly integrated protein complexes; however, mitochondria are also involved in many other functions as well, which, among others, include apoptosis, protein synthesis, and fatty acid oxidation [14,15].”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

2 of the 234 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
van der Bliek, A. M., Sedensky, M. M., & Morgan, P. G.
Affiliations
  • Department of Biological Chemistry, Jonsson Comprehensive Cancer Center and Molecular Biology Institute, David Geffen School of Medicine at UCLA, Los Angeles, California 90024
  • University of Washington (US)
  • Department of Anesthesiology and Pain Medicine, University of Washington and Center for Developmental Therapeutics, Seattle Children’s Research Institute, Washington 98101
Venue
Genetics
Published
2017-10-25
Volume
207
Issue
3
Pages
843-871
ISSN
  • 0016-6731 (ISSN-L)
  • 1943-2631
OpenAlex
W2765579241
Cited by
388
References
234
Citations by year
2026: 22 · 2025: 45 · 2024: 44 · 2023: 58 · 2022: 60 · 2021: 59 · 2020: 62 · 2019: 26 · 2018: 11
FWCI
2.53
Type
journal article
Language
en
Open access
Locations
  • Genetics (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • National Institutes of Health
  • National Institute of General Medical Sciences (U01GM109764, R01GM118514, R01GM105696)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
mitochondria, TCA cycle, oxidative phosphorylation, mitochondrial protein import, mitochondrial biogenesis, mitochondrial fission, mitochondrial fusion, mitophagy, mitochondrial unfolded protein response, stress response, aging
MeSH terms
Animals, Organelle Biogenesis, Citric Acid Cycle, Electron Transport, Mitochondria

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review