Evidence map›Paper›PMID 36846332›Full record

ArticleFrontiers in physiology2023

IGF-1 boosts mitochondrial function by a Ca

Pablo Sánchez-Aguilera, Camila López-Crisosto, Ignacio Norambuena-Soto, Christian Penannen, Jumo Zhu, Nils Bomer, Matijn F Hoes, Peter Van Der Meer, Mario Chiong, B Daan Westenbrink and 1 more

Abstract read
In one paragraph

Article in Frontiers in physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
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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

11 authors.

Pablo Sánchez-AguileraAdvanced Center for Chronic Diseases (ACCDiS), Facultad de Ciencias Químicas y Farmacéuticas, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
Camila López-CrisostoAdvanced Center for Chronic Diseases (ACCDiS), Facultad de Ciencias Químicas y Farmacéuticas, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
Ignacio Norambuena-SotoAdvanced Center for Chronic Diseases (ACCDiS), Facultad de Ciencias Químicas y Farmacéuticas, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
Christian PenannenAdvanced Center for Chronic Diseases (ACCDiS), Facultad de Ciencias Químicas y Farmacéuticas, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
Jumo ZhuDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Nils BomerDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Matijn F HoesDepartment of Clinical Genetics, Maastricht University Medical Center, Maastricht, Netherlands.
Peter Van Der MeerDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Mario ChiongAdvanced Center for Chronic Diseases (ACCDiS), Facultad de Ciencias Químicas y Farmacéuticas, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
B Daan WestenbrinkDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Sergio LavanderoAdvanced Center for Chronic Diseases (ACCDiS), Facultad de Ciencias Químicas y Farmacéuticas, Facultad de Medicina, Universidad de Chile, Santiago, Chile.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A physiological increase in cardiac workload results in adaptive cardiac remodeling, characterized by increased oxidative metabolism and improvements in cardiac performance. Insulin-like growth factor-1 (IGF-1) has been identified as a critical regulator of physiological cardiac growth, but its precise role in cardiometabolic adaptations to physiological stress remains unresolved. Mitochondrial calcium (Ca

Indexed as

human embryonic stem cell derived-cardiomyocytes (hES-CMs)insulin-like growth factor 1 (IGF-1)MCU complexmitochondrial calcium handlingneonatal rat ventricular myocytes (NRVMs)physiological cardiac hypertrophy

Identifiers

PMID36846332
PMCPMC9944404

What OpenQuestion holds

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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.