Evidence map›Paper›PMID 23748424›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2013

Role of mitochondrial dysfunction and altered autophagy in cardiovascular aging and disease: from mechanisms to therapeutics.

Emanuele Marzetti, Anna Csiszar, Debapriya Dutta, Gauthami Balagopal, Riccardo Calvani, Christiaan Leeuwenburgh

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
–field-weighted citation impact
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

104 citing papers in PubMed.

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  20. Non-coding RNAs regulating mitochondrial function in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2023
    Review

44 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

6 authors.

Emanuele MarzettiDepartment of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Rome, Italy;
Anna Csiszar
Debapriya Dutta
Gauthami Balagopal
Riccardo Calvani
Christiaan Leeuwenburgh

Funding

University of Florida Older Americans Independence Center (OAIC)P30AG028740 · NIA · UNIVERSITY OF FLORIDA · PI CHRISTIAAN LEEUWENBURGH · 2007 to 2026
$22.8M
RESOURCE CORE 3: ANALYTICAL COREP30AG028718 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI WEI, JEANNE Y · 2011 to 2015
$5.1M
Apoptosis and Life-Long Caloric RestrictionR01AG021042 · NIA · UNIVERSITY OF FLORIDA · PI LEEUWENBURGH, CHRISTIAAN · 2003 to 2007
$1.7M
Mitophagy: target to improve liver function after ischemia/reperfusion injuryR01DK090115 · NIDDK · UNIVERSITY OF FLORIDA · PI KIM, JAE-SUNG, LEEUWENBURGH, CHRISTIAAN · 2012 to 2015
$1.3M
Vasoprotection by Caloric Restriction Mimetics in AgingK08AG031085 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CSISZAR, ANNA · 2010 to 2012
$518k
NIA NIH HHS 1P30AG028740NIA NIH HHS AG031085NIA NIH HHS K08 AG031085NIA NIH HHS P30 AG028718NIA NIH HHS P30 AG028740NIA NIH HHS R01 AG021042NIA NIH HHS R01-AG21042NIDDK NIH HHS R01-DK090115-01A1
6 · The paper itself

Abstract

Advanced age is associated with a disproportionate prevalence of cardiovascular disease (CVD). Intrinsic alterations in the heart and the vasculature occurring over the life course render the cardiovascular system more vulnerable to various stressors in late life, ultimately favoring the development of CVD. Several lines of evidence indicate mitochondrial dysfunction as a major contributor to cardiovascular senescence. Besides being less bioenergetically efficient, damaged mitochondria also produce increased amounts of reactive oxygen species, with detrimental structural and functional consequences for the cardiovascular system. The age-related accumulation of dysfunctional mitochondrial likely results from the combination of impaired clearance of damaged organelles by autophagy and inadequate replenishment of the cellular mitochondrial pool by mitochondriogenesis. In this review, we summarize the current knowledge about relevant mechanisms and consequences of age-related mitochondrial decay and alterations in mitochondrial quality control in the cardiovascular system. The involvement of mitochondrial dysfunction in the pathogenesis of cardiovascular conditions especially prevalent in late life and the emerging connections with neurodegeneration are also illustrated. Special emphasis is placed on recent discoveries on the role played by alterations in mitochondrial dynamics (fusion and fission), mitophagy, and their interconnections in the context of age-related CVD and endothelial dysfunction. Finally, we discuss pharmacological interventions targeting mitochondrial dysfunction to delay cardiovascular aging and manage CVD.

Indexed as

AutophagyOxidative StressTranslational Research, BiomedicalAge FactorsAgingAnimalsCardiovascular DiseasesCardiovascular SystemHumansMitochondriaMitochondria, HeartMitochondria, MuscleMuscle, Smooth, VascularNeurodegenerative DiseasesNeuronsPrognosisfusion and fissionmitophagyneurodegenerationoxidative stressresveratrol

Identifiers

PMID23748424
PMCPMC3891249

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.