Evidence map›Paper›PMID 22175013›Full record

ArticleJournal of signal transduction2012

Mitochondria-ros crosstalk in the control of cell death and aging.

Saverio Marchi, Carlotta Giorgi, Jan M Suski, Chiara Agnoletto, Angela Bononi, Massimo Bonora, Elena De Marchi, Sonia Missiroli, Simone Patergnani, Federica Poletti and 4 more

Abstract read
In one paragraph

Article in Journal of signal transduction, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 308 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
308citing papers in PubMed, 1 pooled it
–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

308 citing papers in PubMed, 1 synthesis or guideline pooled it.

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248 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

14 authors.

Saverio MarchiDepartment of Experimental and Diagnostic Medicine, Section of General Pathology, Interdisciplinary Center for the Study of Inflammation (ICSI), Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Carlotta Giorgi
Jan M Suski
Chiara Agnoletto
Angela Bononi
Massimo Bonora
Elena De Marchi
Sonia Missiroli
Simone Patergnani
Federica Poletti
Alessandro Rimessi
Jerzy Duszynski
Mariusz R Wieckowski
Paolo Pinton

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) are highly reactive molecules, mainly generated inside mitochondria that can oxidize DNA, proteins, and lipids. At physiological levels, ROS function as "redox messengers" in intracellular signalling and regulation, whereas excess ROS induce cell death by promoting the intrinsic apoptotic pathway. Recent work has pointed to a further role of ROS in activation of autophagy and their importance in the regulation of aging. This review will focus on mitochondria as producers and targets of ROS and will summarize different proteins that modulate the redox state of the cell. Moreover, the involvement of ROS and mitochondria in different molecular pathways controlling lifespan will be reported, pointing out the role of ROS as a "balance of power," directing the cell towards life or death.

Identifiers

PMID22175013
PMCPMC3235816

What OpenQuestion holds

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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.