Evidence map›Paper›PMID 38099846›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2024

Aging-induced mitochondrial dysfunction: two distinct populations of mitochondria versus a combined population.

Qun Chen, Jeremy Thompson, Ying Hu, Edward J Lesnefsky

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
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.

Qun ChenDivision of Cardiology, Department of Medicine, Virginia Commonwealth University, Richmond, Virginia, United States.ORCID 0000-0001-5683-7844
Jeremy ThompsonDivision of Cardiology, Department of Medicine, Virginia Commonwealth University, Richmond, Virginia, United States.
Ying HuDivision of Cardiology, Department of Medicine, Virginia Commonwealth University, Richmond, Virginia, United States.
Edward J LesnefskyDivision of Cardiology, Department of Medicine, Virginia Commonwealth University, Richmond, Virginia, United States.
Virginia Commonwealth University · US

Funding

Metformin Therapy for Ischemic Insult and Reperfusion Injury in AgingR33AG071249 · NIA · VIRGINIA COMMONWEALTH UNIVERSITY · PI LESNEFSKY, EDWARD J, LI, JI · 2023 to 2024
$761k
Aged rat heart mitochondrial dysfunction: proteome and lipidome dynamicsR21AG049461 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI HOPPEL, CHARLES LESLIE · 2015 to 2015
$238k
Reduction of cardiac injury by targeting damaged mitochondria during reperfusionI01BX001355 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI LESNEFSKY, EDWARD J · 2012 to 2025
–
BLRD VA I01 BX001355NIA NIH HHS R21 AG049461NIA NIH HHS R33 AG071249
6 · The paper itself

Abstract

Mitochondrial function in aged hearts is impaired, and studies of isolated mitochondria are commonly used to assess their function. The two populations of cardiac mitochondria, subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM), are affected by aging. However, the yield of these mitochondria, particularly SSM, is limited in the mouse heart because of the smaller heart size. To address this issue, the authors developed a method to isolate a mixed population (MIX) of SSM and IFM mitochondria from a single mouse heart. The aim of the study was to compare the mitochondrial function between SSM, IFM, and the MIX population from young and aged mouse hearts. The MIX population had a higher yield of total protein and citrate synthase activity from both young and aged hearts compared with the individual yields of SSM or IFM. Oxidative phosphorylation (OXPHOS) decreased in aged SSM and IFM compared with young SSM and IFM, as well as in the MIX population isolated from aged hearts compared with young hearts, when using complex I or IV substrates. Furthermore, aging barely affected the sensitivity to mitochondrial permeability transition pore (MPTP) opening in SSM, whereas the sensitivity was increased in IFM isolated from aged hearts and in the MIX population from aged hearts compared with the corresponding populations isolated from young hearts. These results suggest that mitochondrial dysfunction exists in aged hearts and the isolation of a MIX population of mitochondria from the mouse heart is a potential approach to studying mitochondrial function in the mouse heart.

Indexed as

HeartMitochondrial DiseasesAgingAnimalsMiceMitochondria, HeartOxidative Phosphorylationagingcomplex Iinterfibrillar mitochondriaoxidative phosphorylationsubsarcolemmal mitochondria

Identifiers

PMID38099846
PMCPMC11219051
OpenAlexW4389783342

What OpenQuestion holds

Textmetadata
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.