Evidence map›Paper›PMID 10995435›Full record

ArticleThe Journal of cell biology2000

Desmin cytoskeleton linked to muscle mitochondrial distribution and respiratory function.

D J Milner, M Mavroidis, N Weisleder, Y Capetanaki

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

167 citing papers in PubMed, 379 citations in OpenAlex.

  1. Review
  2. Increased Expression of Desmin and Vimentin Impairs Mitochondrial Function and Reduces Contractility via G0S2 in Bladder Smooth Muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  9. The Approximate Subcutaneous LDMolecules (Basel, Switzerland) · 2026
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  11. Review
  12. The intermediate filament protein GFAP regulates mitochondrial fission in astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  14. Review
  15. Article
  16. LSMEM2, Localized at the Neuromuscular Junction, Modulates Mitochondrial Integration in Skeletal Muscles.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  19. Colonocyte keratins stabilize mitochondria and contribute to mitochondrial energy metabolism.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  20. Article

107 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

D J MilnerDepartment of Molecular and Cell Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
M Mavroidis
N Weisleder
Y Capetanaki
Baylor College of Medicine · US

Funding

FUNCTION OF INTERMEDIATE FILAMENTS IN MUSCLER01AR039617 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI CAPETANAKI, YASSEMI · 1988 to 2001
$544k
NIAMS NIH HHS R01 AR039617
6 · The paper itself

Abstract

Ultrastructural studies have previously suggested potential association of intermediate filaments (IFs) with mitochondria. Thus, we have investigated mitochondrial distribution and function in muscle lacking the IF protein desmin. Immunostaining of skeletal muscle tissue sections, as well as histochemical staining for the mitochondrial marker enzymes cytochrome C oxidase and succinate dehydrogenase, demonstrate abnormal accumulation of subsarcolemmal clumps of mitochondria in predominantly slow twitch skeletal muscle of desmin-null mice. Ultrastructural observation of desmin-null cardiac muscle demonstrates in addition to clumping, extensive mitochondrial proliferation in a significant fraction of the myocytes, particularly after work overload. These alterations are frequently associated with swelling and degeneration of the mitochondrial matrix. Mitochondrial abnormalities can be detected very early, before other structural defects become obvious. To investigate related changes in mitochondrial function, we have analyzed ADP-stimulated respiration of isolated muscle mitochondria, and ADP-stimulated mitochondrial respiration in situ using saponin skinned muscle fibers. The in vitro maximal rates of respiration in isolated cardiac mitochondria from desmin-null and wild-type mice were similar. However, mitochondrial respiration in situ is significantly altered in desmin-null muscle. Both the maximal rate of ADP-stimulated oxygen consumption and the dissociation constant (K(m)) for ADP are significantly reduced in desmin-null cardiac and soleus muscle compared with controls. Respiratory parameters for desmin-null fast twitch gastrocnemius muscle were unaffected. Additionally, respiratory measurements in the presence of creatine indicate that coupling of creatine kinase and the adenine translocator is lost in desmin-null soleus muscle. This coupling is unaffected in cardiac muscle from desmin-null animals. All of these studies indicate that desmin IFs play a significant role in mitochondrial positioning and respiratory function in cardiac and skeletal muscle.

Indexed as

Adenosine DiphosphateAnimalsCardiomyopathiesCell RespirationDesminEnergy MetabolismIntermediate FilamentsMiceMice, KnockoutMicroscopy, ElectronMitochondriaMuscle Fibers, SkeletalMuscle, SkeletalMyocardiumAdenosine DiphosphateDesmin

Identifiers

PMID10995435
PMCPMC2150713
OpenAlexW1987137066

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.