Evidence map›Paper›PMID 35218410›Full record

ArticleCellular and molecular life sciences : CMLS2022

ROS-induced PADI2 downregulation accelerates cellular senescence via the stimulation of SASP production and NFκB activation.

Hyun-Jung Kim, Woo-Jin Kim, Hye-Rim Shin, Hee-In Yoon, Jae-I Moon, Eunji Lee, Jin-Muk Lim, Young-Dan Cho, Mi-Hye Lee, Hong-Gee Kim and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 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

11 authors at 3 institutions in 3 countries.

Hyun-Jung KimDepartment of Molecular Genetics & Dental Pharmacology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea.ORCID http://orcid.org/0000-0002-5360-1809
Woo-Jin KimDepartment of Molecular Genetics & Dental Pharmacology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea.
Hye-Rim ShinDepartment of Molecular Genetics & Dental Pharmacology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea.
Hee-In YoonDepartment of Molecular Genetics & Dental Pharmacology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea.
Jae-I MoonDepartment of Molecular Genetics & Dental Pharmacology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea.
Eunji LeeDepartment of Molecular Genetics & Dental Pharmacology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea.
Jin-Muk LimBiomedical Knowledge Engineering Laboratory, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea.
Young-Dan ChoDepartment of Periodontology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea.
Mi-Hye LeeDepartment of Biology and Center for Cell Reprogramming, Georgetown University, Washington, DC, USA.
Hong-Gee KimBiomedical Knowledge Engineering Laboratory, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea.
Hyun-Mo RyooDepartment of Molecular Genetics & Dental Pharmacology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, South Korea. hmryoo@snu.ac.kr.ORCID http://orcid.org/0000-0001-6769-8341
Seoul National University Dental Hospital · KRSeoul National University · KRGeorgetown University · US

Funding

National Research Foundation of Korea 2017R1A2B3011778National Research Foundation of Korea 2017R1A4A1014584National Research Foundation of Korea 2020R1A2B5B02002658National Research Foundation of Korea 2020R1A4A1019423National Research Foundation of Korea 2021R1A2C1007715
6 · The paper itself

Abstract

Cellular senescence is closely related to tissue aging including bone. Bone homeostasis is maintained by the tight balance between bone-forming osteoblasts and bone-resorbing osteoclasts, but it undergoes deregulation with age, causing age-associated osteoporosis, a main cause of which is osteoblast dysfunction. Oxidative stress caused by the accumulation of reactive oxygen species (ROS) in bone tissues with aging can accelerate osteoblast senescence and dysfunction. However, the regulatory mechanism that controls the ROS-induced senescence of osteoblasts is poorly understood. Here, we identified Peptidyl arginine deiminase 2 (PADI2), a post-translational modifying enzyme, as a regulator of ROS-accelerated senescence of osteoblasts via RNA-sequencing and further functional validations. PADI2 downregulation by treatment with H

Indexed as

AnimalsCell DifferentiationCell LineCellular SenescenceChemokine CCL2Chemokine CCL5Chemokine CCL7Chemokines, CCDNA DamageDown-RegulationHydrogen PeroxideMiceNF-kappa BOsteoblastsProtein-Arginine Deiminase Type 2Reactive Oxygen SpeciesChemokine CCL2Chemokine CCL5Chemokine CCL7Chemokines, CCHydrogen PeroxideNF-kappa BPadi2 protein, mouseProtein-Arginine Deiminase Type 2Reactive Oxygen SpeciesRNA, Small InterferingNFκBOsteoblastPeptidyl arginine deiminase 2Reactive oxygen speciesSenescenceSenescence-associated secretory phenotype

Identifiers

PMID35218410
PMCPMC8882118
OpenAlexW4214682607

What OpenQuestion holds

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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.