Evidence map›Paper›PMID 33484871›Full record

ArticleMitochondrion2021

Mitochondria and early-life adversity.

Emily K Zitkovsky, Teresa E Daniels, Audrey R Tyrka

Open access · greenAbstract read
In one paragraph

Article in Mitochondrion, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
13.7field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 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

3 authors at 1 institution in 1 country.

Emily K ZitkovskyMood Disorders Research Program and Laboratory for Clinical and Translational Neuroscience, Butler Hospital, 345 Blackstone Boulevard, Providence, RI 02906, USA; Alpert Medical School of Brown University, 222 Richmond St, Providence, RI 02903, USA. Electronic address: emily_zitkovsky@brown.edu.
Teresa E DanielsMood Disorders Research Program and Laboratory for Clinical and Translational Neuroscience, Butler Hospital, 345 Blackstone Boulevard, Providence, RI 02906, USA; Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, 345 Blackstone Boulevard, Providence, RI 02906, USA. Electronic address: teresa_daniels@brown.edu.
Audrey R TyrkaMood Disorders Research Program and Laboratory for Clinical and Translational Neuroscience, Butler Hospital, 345 Blackstone Boulevard, Providence, RI 02906, USA; Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, 345 Blackstone Boulevard, Providence, RI 02906, USA. Electronic address: audrey_tyrka@brown.edu.
Providence College · US

Funding

Promoting Research Training During Psychiatry ResidencyR25MH101076 · NIMH · BROWN UNIVERSITY · PI AUDREY TYRKA · 2013 to 2026
$2.8M
Risk Profiles and Mechanisms of Disease in Maltreated ChildrenR01HD086487 · NICHD · BUTLER HOSPITAL (PROVIDENCE, RI) · PI TYRKA, AUDREY · 2016 to 2020
$2.8M
Early Life Stress: Epigenetic Regulation of Endocrine and Immune PathwaysR01MH101107 · NIMH · BUTLER HOSPITAL (PROVIDENCE, RI) · PI TYRKA, AUDREY · 2014 to 2018
$2.6M
NICHD NIH HHS R01 HD086487NIMH NIH HHS R01 MH101107NIMH NIH HHS R25 MH101076
6 · The paper itself

Abstract

Early-life adversity (ELA), which includes maltreatment, neglect, or severe trauma in childhood, increases the life-long risk for negative health outcomes. Mitochondria play a key role in the stress response and may be an important mechanism by which stress is transduced into biological risk for disease. By responding to cues from stress-signaling pathways, mitochondria interact dynamically with physiological stress responses coordinated by the central nervous, endocrine, and immune systems. Preclinical evidence suggests that alterations in mitochondrial function and structure are linked to both early stress and systemic biological dysfunction. Early clinical studies support that increased mitochondrial DNA content and altered cellular energy demands may be present in individuals with a history of ELA. Further research should investigate mitochondria as a potential therapeutic target following ELA.

Indexed as

Stress, PhysiologicalAdverse Childhood ExperiencesAnimalsCentral Nervous SystemEndocrine SystemHumansImmune SystemMitochondriaEarly-life adversityMechanismsMitochondriaStressTrauma

Identifiers

PMID33484871
PMCPMC8172448
OpenAlexW3122533124

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.