Evidence map›Paper›PMID 33802550›Full record

ReviewCells2021

Cell Death and Inflammation: The Role of Mitochondria in Health and Disease.

Anna Picca, Riccardo Calvani, Hélio José Coelho-Junior, Emanuele Marzetti

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 2 pooled it
11.8field-weighted citation impact, top 1% 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

100 citing papers in PubMed, 2 syntheses or guidelines pooled it, 189 citations in OpenAlex.

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  13. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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40 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 2 institutions in 2 countries.

Anna PiccaFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.ORCID 0000-0001-7032-3487
Riccardo CalvaniFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.ORCID 0000-0001-5472-2365
Hélio José Coelho-JuniorUniversità Cattolica del Sacro Cuore, Institute of Internal Medicine and Geriatrics, 00168 Rome, Italy.ORCID 0000-0001-7482-9514
Emanuele MarzettiFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.ORCID 0000-0001-9567-6983
Stockholm University · SEUniversità Cattolica del Sacro Cuore · IT

Funding

Centro Studi Achille e Linda Lorenzon N/AUniversità Cattolica del Sacro Cuore D1.2020
6 · The paper itself

Abstract

Mitochondria serve as a hub for a multitude of vital cellular processes. To ensure an efficient deployment of mitochondrial tasks, organelle homeostasis needs to be preserved. Mitochondrial quality control (MQC) mechanisms (i.e., mitochondrial dynamics, biogenesis, proteostasis, and autophagy) are in place to safeguard organelle integrity and functionality. Defective MQC has been reported in several conditions characterized by chronic low-grade inflammation. In this context, the displacement of mitochondrial components, including mitochondrial DNA (mtDNA), into the extracellular compartment is a possible factor eliciting an innate immune response. The presence of bacterial-like CpG islands in mtDNA makes this molecule recognized as a damaged-associated molecular pattern by the innate immune system. Following cell death-triggering stressors, mtDNA can be released from the cell and ignite inflammation via several pathways. Crosstalk between autophagy and apoptosis has emerged as a pivotal factor for the regulation of mtDNA release, cell's fate, and inflammation. The repression of mtDNA-mediated interferon production, a powerful driver of immunological cell death, is also regulated by autophagy-apoptosis crosstalk. Interferon production during mtDNA-mediated inflammation may be exploited for the elimination of dying cells and their conversion into elements driving anti-tumor immunity.

Indexed as

AlarminsApoptosisDNA, MitochondrialGene Expression RegulationHomeostasisHumansImmunity, InnateInflammationInterferonsMitochondriaMitochondrial DynamicsMitophagyNeoplasmsOxidative StressReactive Oxygen SpeciesSignal TransductionAlarminsDNA, MitochondrialInterferonsReactive Oxygen Speciesapoptosisdamage-associated molecular patterns (DAMPs)immunogenic cell deathinnate immunitymitochondrial dynamicsmitochondrial dysfunctionmitochondrial quality control (MQC)mitophagyoxidative stressreactive oxygen species (ROS)

Identifiers

PMID33802550
PMCPMC7998762
OpenAlexW3134630041

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.