Evidence map›Paper›PMID 31941960›Full record

ArticleScientific reports2020

Tuning mitochondrial structure and function to criticality by fluctuation-driven mechanotransduction.

Erzsébet Bartolák-Suki, Béla Suki

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Network-Associated Mechanotransduction in Health and Disease.Results and problems in cell differentiation · 2026
    Review
  2. Mitochondrial Adaptation to Mechanical Stress in Cardiac Ageing and Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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  13. Common methods in mitochondrial research (Review).International journal of molecular medicine · 2022
    Article
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  16. Review
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  20. Mitochondrial Dysfunction: Cause or Consequence of Vascular Calcification?Frontiers in cell and developmental biology · 2021
    Review
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

2 authors at 1 institution in 1 country.

Erzsébet Bartolák-SukiDepartment of Biomedical Engineering, Boston University, Boston, MA, 02215, United States. ebartola@bu.edu.ORCID http://orcid.org/0000-0003-1007-6394
Béla SukiDepartment of Biomedical Engineering, Boston University, Boston, MA, 02215, United States. bsuki@bu.edu.ORCID http://orcid.org/0000-0002-9720-1006
Boston University · US

Funding

A multi-scale computational model of the extracellular matrix of the lungU01HL139466 · NHLBI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI SUKI, BELA · 2018 to 2022
$3.9M
Pulmonary arterial endothelial stiffness and shear-stress induced signalingR21HL126040 · NHLBI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI SUKI, BELA · 2015 to 2016
$451k
Advanced laser scanning confocal microscope for multiple usersS10OD024993 · OD · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI MERTZ, JEROME · 2018 to 2018
$448k
NHLBI NIH HHS R21 HL126040
6 · The paper itself

Abstract

Cells in vascular walls are exposed to blood pressure variability (BPV)-induced cycle-by-cycle fluctuations in mechanical forces which vary considerably with pathology. For example, BPV is elevated in hypertension but reduced under anesthesia. We hypothesized that the extent of mechanical fluctuations applied to vascular smooth muscle cells (VSMCs) regulates mitochondrial network structure near the percolation transition, which also influences ATP and reactive oxygen species (ROS) production. We stretched VSMCs in culture with cycle-by-cycle variability in area strain ranging from no variability (0%), as in standard laboratory conditions, through abnormally small (6%) and physiological (25%) to pathologically high (50%) variability mimicking hypertension, superimposed on 0.1 mean area strain. To explore how oxidative stress and ATP-dependent metabolism affect mitochondria, experiments were repeated in the presence of hydrogen peroxide and AMP-PNP, an ATP analog and competitive inhibitor of ATPases. Physiological 25% variability maintained activated mitochondrial cluster structure at percolation with a power law distribution and exponent matching the theoretical value in 2 dimensions. The 25% variability also maximized ATP and minimized cellular and mitochondrial ROS production via selective control of fission and fusion proteins (mitofusins, OPA1 and DRP1) as well as through stretch-sensitive regulation of the ATP synthase and VDAC1, the channel that releases ATP into the cytosol. Furthermore, pathologically low or high variability moved mitochondria away from percolation which reduced the effectiveness of the electron transport chain by lowering ATP and increasing ROS productions. We conclude that normal BPV is required for maintaining optimal mitochondrial structure and function in VSMCs.

Indexed as

Adenosine TriphosphateAnimalsCattleCells, CulturedMechanotransduction, CellularMitochondriaMitochondrial ProteinsMuscle, Smooth, VascularMyocytes, Smooth MuscleOxidation-ReductionOxidative StressReactive Oxygen SpeciesAdenosine TriphosphateMitochondrial ProteinsReactive Oxygen Species

Identifiers

PMID31941960
PMCPMC6962425
OpenAlexW2999577120

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.