Evidence map›Paper›PMID 37310873›Full record

ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2023

Interleukin-6 Drives Mitochondrial Dysregulation and Accelerates Physical Decline: Insights From an Inducible Humanized IL-6 Knock-In Mouse Model.

Lolita S Nidadavolu, Caglar Cosarderelioglu, Alessandra Merino Gomez, Yuqiong Wu, Taylor Bopp, Cissy Zhang, Tu Nguyen, Ruth Marx-Rattner, Huanle Yang, Corina Antonescu and 10 more

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In one paragraph

Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
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

20 authors at 1 institution in 1 country.

Lolita S NidadavoluDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0003-2433-0728
Caglar CosardereliogluDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-7560-1287
Alessandra Merino GomezDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Yuqiong WuDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Taylor BoppDepartment of Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Cissy ZhangDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Tu NguyenDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Ruth Marx-RattnerDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Huanle YangDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Corina AntonescuDepartment of Genetic Medicine, John Hopkins University School of Medicine, Baltimore, Maryland, USA.
Liliana FloreaDepartment of Genetic Medicine, John Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0001-8124-2324
Conover C TalbotInstitute for Basic Biomedical Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Barbara SmithDepartment of Cell Biology, Imaging Facility, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
D Brian FosterDivision of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.
Jennifer E FairmanDivision of Cellular and Molecular Medicine, Department of Art as Applied to Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Gayane YenokyanJohns Hopkins Biostatistics Center, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.ORCID 0000-0003-1482-5612
Tae ChungDepartment of Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Anne LeDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jeremy D WalstonDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Peter M AbadirDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Johns Hopkins University · US

Funding

Technological Assessment and Solutions Core - RC4P30AG021334 · NIA · JOHNS HOPKINS UNIVERSITY · PI Jeremy D Walston · 2003 to 2026
$33.2M
Retinoid Metabolism in the Adult Heart and Heart FailureR01HL164478 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI D Brian Foster, MAUREEN A KANE · 2023 to 2026
$2.8M
Age Related Change in Mitochondrial Angiotensin System and Mitochondrial DeclineR01AG046441 · NIA · JOHNS HOPKINS UNIVERSITY · PI ABADIR, PETER M. · 2014 to 2018
$2.3M
Targeting Metabo-Redox Network Vulnerability in Heart Failure and Sudden DeathR01HL134821 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI FOSTER, D BRIAN, O'ROURKE, BRIAN · 2018 to 2021
$2.1M
Computational Methods to Characterize Alternative Splicing from Massive Collections of RNA-seq DataR01GM129085 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI FLOREA, LILIANA D · 2019 to 2022
$1.5M
NHLBI NIH HHS R01 HL134821NHLBI NIH HHS R01 HL164478NIA NIH HHS P30 AG021334NIA NIH HHS R01 AG046441NIGMS NIH HHS R01 GM129085NIH HHS R01AG046441
6 · The paper itself

Abstract

Chronic activation of inflammatory pathways (CI) and mitochondrial dysfunction are independently linked to age-related functional decline and early mortality. Interleukin 6 (IL-6) is among the most consistently elevated chronic activation of inflammatory pathways markers, but whether IL-6 plays a causative role in this mitochondrial dysfunction and physical deterioration remains unclear. To characterize the role of IL-6 in age-related mitochondrial dysregulation and physical decline, we have developed an inducible human IL-6 (hIL-6) knock-in mouse (TetO-hIL-6mitoQC) that also contains a mitochondrial-quality control reporter. Six weeks of hIL-6 induction resulted in upregulation of proinflammatory markers, cell proliferation and metabolic pathways, and dysregulated energy utilization. Decreased grip strength, increased falls off the treadmill, and increased frailty index were also observed. Further characterization of skeletal muscles postinduction revealed an increase in mitophagy, downregulation of mitochondrial biogenesis genes, and an overall decrease in total mitochondrial numbers. This study highlights the contribution of IL-6 to mitochondrial dysregulation and supports a causal role of hIL-6 in physical decline and frailty.

Indexed as

FrailtyInterleukin-6AnimalsDisease Models, AnimalHumansMiceMitochondriaMuscle, SkeletalInterleukin-6InflammationMitochondria dysregulationPhysical decline

Identifiers

PMID37310873
PMCPMC10562892
OpenAlexW4380415296

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.