Evidence map›Paper›PMID 42845619›Full record

ArticleResearch square2026

A novel multisystem approach uncovers conserved mitochondrial complex I disease phenotypes and suppressors.

Natascia Ventura, Lena Jentsch, Silvia Maglioni, Caleb Jerred, Tyler O'Hara, Eirini Mytilinaiou, Jimena Ruiz, Yulia Schaumkessel, Laura Schroeter, Jiwon Jung and 9 more

Abstract readPreprint
In one paragraph

Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

19 authors.

Natascia VenturaHeinrich Heine University Düsseldorf.ORCID 0000-0001-8718-4321
Lena JentschUniversity Hospital Duesseldorf. Heinrich Heine University.
Silvia MaglioniUniversity Hospital Duesseldorf. Heinrich Heine University.
Caleb JerredHeinrich Heine University Düsseldorf.
Tyler O'HaraThe Children's Hospital of Philadelphia.
Eirini MytilinaiouNational and Kapodistrian University of Athens.
Jimena RuizWashington State University.
Yulia SchaumkesselHeinrich Heine University Dusseldorf.ORCID 0009-0000-6016-3301
Laura SchroeterUniversity Hospital Duesseldorf. Heinrich Heine University.
Jiwon JungLeibniz Research Institute for Environmental Medicine.
Nikola YotovLeibniz Research Institute for Environmental Medicine.ORCID 0009-0005-1287-5474
Johanna HoffmannLeibniz Research Institute for Environmental Medicine.
Kai KremersLeibniz Research Institute for Environmental Medicine.ORCID 0009-0001-5884-1756
Andrea RossiIUF-Leibniz Research Institute for Environmental Medicine.ORCID 0000-0001-5863-6448
Andreas ReichertInstitute of Biochemistry and Molecular Biology I, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University.ORCID 0000-0001-9340-3113
Jennifer WattsWashington State University Pullman.ORCID 0000-0003-4349-0639
Konstantinos PalikarasNational and Kapodistrian University of Athens.ORCID 0000-0001-6992-5560
Suraiya HaroonChildren's Hospital of Philadelphia.ORCID 0000-0001-5575-4609
Alessandro PrigioneUniversity Hospital Duesseldorf. Heinrich Heine University.

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Molecular mechanisms of ferroptosis induction throughout germline development and agingR35GM152060 · NIGMS · WASHINGTON STATE UNIVERSITY · PI Jennifer L Watts · 2024 to 2026
$1.1M
NIGMS NIH HHS R35 GM152060NIH HHS P40 OD010440
6 · The paper itself

Abstract

Mitochondriopathies are a large group of pathological conditions characterized by dysfunction of tissues and organs with high energy needs such as the brain, heart, and skeletal muscles, which highly rely on functional mitochondrial oxidative phosphorylation (OXPHOS). The vast majority of these disorders are ascribed to mutations in nuclear or mitochondrial encoded subunits of complex I (CI), the largest OXPHOS complex. In this study, we develop a multisystemic pipeline for CI-associated disease based on new approach methods (NAMs), which includes non-mammalian models, namely

Indexed as

Brain organoidsC. elegansComplex I deficiencyLeigh syndromeLuteinMitochondriaModel organismsNAMVitamin B12 (cobalamin)Zebrafish

Identifiers

PMID42845619
PMCPMC13640897

What OpenQuestion holds

Textmetadata
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.