Evidence map›Paper›PMID 34087956›Full record

ArticleAging cell2021

Nucleotide-binding domain and leucine-rich-repeat-containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung-like changes.

Hyeon Jun Shin, Sang-Hun Kim, Hong-Jai Park, Min-Sun Shin, Insoo Kang, Min-Jong Kang

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Aging gene signature of memory CD8Immunity & ageing : I & A · 2023
    Article
  7. Article
  8. Extracellular HSP90α promotes cellular senescence by modulating TGF-β signaling in pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  9. Article
  10. 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

6 authors at 1 institution in 1 country.

Hyeon Jun ShinSection of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Sang-Hun KimSection of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Hong-Jai ParkSection of Rheumatology, Allergy and Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Min-Sun ShinSection of Rheumatology, Allergy and Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Insoo KangSection of Rheumatology, Allergy and Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Min-Jong KangSection of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.ORCID 0000-0003-3245-144X
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
The reduction of NLRX1 and its role in pulmonary agingR01AG053495 · NIA · YALE UNIVERSITY · PI KANG, MIN-JONG · 2016 to 2020
$1.7M
Role of NLRX1 in cigarette smoke-induced pulmonary inflammation and remodelingR01HL130283 · NHLBI · YALE UNIVERSITY · PI KANG, MIN-JONG · 2016 to 2019
$1.7M
NCATS NIH HHS UL1 TR001863NHLBI NIH HHS R01 HL130283NIA NIH HHS R01 AG053495
6 · The paper itself

Abstract

Mitochondrial dysfunction has long been implicated to have a causative role in organismal aging. A mitochondrial molecule, nucleotide-binding domain and leucine-rich-repeat-containing protein X1 (NLRX1), represents the only NLR family member that targets this cellular location, implying that NLRX1 probably establishes a fundamental link between mitochondrial functions and cellular physiology. However, the significance of NLRX1 function in cellular senescence, a key conceptual constituent in aging biology, is yet to be defined. Here, we demonstrate that molecular hallmarks involved in aging biology including NAD

Indexed as

AgingAnimalsCellular SenescenceHumansLungMiceMitochondrial ProteinsNLR ProteinsSirolimusMitochondrial ProteinsNLR ProteinsNLRX1 protein, mouseSirolimuscellular senescencelung agingmTOR (mechanistic target of rapamycin)NAD+ (nicotinamide adenine dinucleotide)NLRX1 (nucleotide-binding domain and leucine-rich-repeat-containing protein X1)

Identifiers

PMID34087956
PMCPMC8282248
OpenAlexW3165503835

What OpenQuestion holds

Textmetadata
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.