Evidence map›Paper›PMID 28452964›Full record

ReviewInternational journal of molecular sciences2017

Fueling Inflamm-Aging through Mitochondrial Dysfunction: Mechanisms and Molecular Targets.

Anna Picca, Angela Maria Serena Lezza, Christiaan Leeuwenburgh, Vito Pesce, Riccardo Calvani, Francesco Landi, Roberto Bernabei, Emanuele Marzetti

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

118 citing papers in PubMed, 185 citations in OpenAlex.

  1. Trial
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  9. Inflammaging and Cardiovascular Risk in Old Women.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2026
    Review
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  11. Article
  12. Review
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  15. Article
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  19. Article
  20. Mitochondrial Membrane Potential of CD8Journal of clinical and translational hepatology · 2025
    Article

58 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

8 authors at 3 institutions in 2 countries.

Anna PiccaDepartment of Geriatrics, Neuroscience and Orthopedics, Catholic University of the Sacred Heart School of Medicine, 00168 Rome, Italy. anna.picca1@gmail.com.
Angela Maria Serena LezzaDepartment of Biosciences, Biotechnology and Biopharmaceutics, University of Bari, 70125 Bari, Italy. angelamariaserena.lezza@uniba.it.
Christiaan LeeuwenburghDepartment of Aging and Geriatric Research, Institute on Aging, Division of Biology of Aging, University of Florida, Gainesville, FL 32611, USA. cleeuwen@ufl.edu.
Vito PesceDepartment of Biosciences, Biotechnology and Biopharmaceutics, University of Bari, 70125 Bari, Italy. vito.pesce@uniba.it.
Riccardo CalvaniDepartment of Geriatrics, Neuroscience and Orthopedics, Catholic University of the Sacred Heart School of Medicine, 00168 Rome, Italy. riccardo.calvani@gmail.com.
Francesco LandiDepartment of Geriatrics, Neuroscience and Orthopedics, Catholic University of the Sacred Heart School of Medicine, 00168 Rome, Italy. francesco.landi@unicatt.it.
Roberto BernabeiDepartment of Geriatrics, Neuroscience and Orthopedics, Catholic University of the Sacred Heart School of Medicine, 00168 Rome, Italy. roberto.bernabei@unicatt.it.
Emanuele MarzettiDepartment of Geriatrics, Neuroscience and Orthopedics, Catholic University of the Sacred Heart School of Medicine, 00168 Rome, Italy. emarzetti@live.com.
Università Cattolica del Sacro Cuore · ITUniversity of Bari Aldo Moro · ITUniversity of Florida · US

Funding

University of Florida Older Americans Independence Center (OAIC)P30AG028740 · NIA · UNIVERSITY OF FLORIDA · PI Peihua Qiu · 2007 to 2026
$22.8M
NIA NIH HHS P30 AG028740
6 · The paper itself

Abstract

Among the complex determinants of aging, mitochondrial dysfunction has been in the spotlight for a long time. As the hub for many cellular functions, the maintenance of an adequate pool of functional mitochondria is crucial for tissue homeostasis. Their unique role in energy supply makes these organelles essential, especially in those tissues strictly dependent on oxidative metabolism. Mitochondrial quality control (MQC) is ensured by pathways related to protein folding and degradation as well as by processes involving the entire organelle, such as biogenesis, dynamics, and mitophagy. Dysfunctional MQC, oxidative stress and inflammation are hallmarks of senescence and chronic degenerative diseases. One of the consequences of age-related failing MQC and oxidative stress is the release of mitochondria-derived damage-associated molecular patterns (DAMPs). Through their bacterial ancestry, these molecules contribute to mounting an inflammatory response by interacting with receptors similar to those involved in pathogen-associated responses. Mitochondrial DAMPs, especially cell-free mitochondrial DNA, have recently become the subject of intensive research because of their possible involvement in conditions associated with inflammation, such as aging and degenerative diseases. Here, we review the contribution of mitochondrial DAMPs to inflammation and discuss some of the mechanisms at the basis of their generation.

Indexed as

AgingInflammationAlarminsDNA, MitochondrialHumansMitochondriaMitochondrial DynamicsMitophagyOxidative StressAlarminsDNA, Mitochondrialdamage-associated molecular patterns (DAMPs)inflammasomemitochondrial biogenesismitochondrial dynamicsmitochondrial quality control (MQC)mitophagysterile inflammationTFAM

Identifiers

PMID28452964
PMCPMC5454846
OpenAlexW2608624623

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.