Evidence map›Paper›PMID 35203322›Full record

ReviewCells2022

Circulating Mitochondrial DNA and Inter-Organelle Contact Sites in Aging and Associated Conditions.

Anna Picca, Flora Guerra, Riccardo Calvani, Roberta Romano, Hélio José Coelho-Junior, Francesco P Damiano, Cecilia Bucci, Emanuele Marzetti

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 25 citations in OpenAlex.

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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 1 country.

Anna PiccaFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.ORCID 0000-0001-7032-3487
Flora GuerraDepartment of Biological and Environmental Sciences and Technologies, Università del Salento, 73100 Lecce, Italy.ORCID 0000-0003-3379-7469
Riccardo CalvaniFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.ORCID 0000-0001-5472-2365
Roberta RomanoDepartment of Biological and Environmental Sciences and Technologies, Università del Salento, 73100 Lecce, Italy.ORCID 0000-0002-4987-3561
Hélio José Coelho-JuniorDepartment of Geriatrics and Orthopedics, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.ORCID 0000-0001-7482-9514
Francesco P DamianoFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.
Cecilia BucciDepartment of Biological and Environmental Sciences and Technologies, Università del Salento, 73100 Lecce, Italy.ORCID 0000-0002-6232-6183
Emanuele MarzettiFondazione Policlinico Universitario "Agostino Gemelli" IRCCS, 00168 Rome, Italy.ORCID 0000-0001-9567-6983
Agostino Gemelli University Polyclinic · ITUniversity of Salento · ITUniversità Cattolica del Sacro Cuore · IT

Funding

Catholic University of the Sacred Heart D1.2020Centro Studi Achille e Linda Lorenzon N/AMinistry of Education, Universities and Research DM 587, 08/08/2018; CIB N. 112/19
6 · The paper itself

Abstract

Mitochondria are primarily involved in cell bioenergetics, regulation of redox homeostasis, and cell death/survival signaling. An immunostimulatory property of mitochondria has also been recognized which is deployed through the extracellular release of entire or portioned organelle and/or mitochondrial DNA (mtDNA) unloading. Dynamic homo- and heterotypic interactions involving mitochondria have been described. Each type of connection has functional implications that eventually optimize mitochondrial activity according to the bioenergetic demands of a specific cell/tissue. Inter-organelle communications may also serve as molecular platforms for the extracellular release of mitochondrial components and subsequent ignition of systemic inflammation. Age-related chronic inflammation (inflamm-aging) has been associated with mitochondrial dysfunction and increased extracellular release of mitochondrial components-in particular, cell-free mtDNA. The close relationship between mitochondrial dysfunction and cellular senescence further supports the central role of mitochondria in the aging process and its related conditions. Here, we provide an overview of (1) the mitochondrial genetic system and the potential routes for generating and releasing mtDNA intermediates; (2) the pro-inflammatory pathways elicited by circulating mtDNA; (3) the participation of inter-organelle contacts to mtDNA homeostasis; and (4) the link of these processes with senescence and age-associated conditions.

Indexed as

DNA, MitochondrialMitochondriaHumansInflammationMitochondrial MembranesDNA, Mitochondrialexosomesextracellular vesiclesinflamm-agingmitochondrial damagemitochondrial-derived vesiclesmitochondrial dynamicsmitochondrial-lysosomal axismitophagyoxidative stresssenescence

Identifiers

PMID35203322
PMCPMC8870554
OpenAlexW4213168523

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.