Evidence map›Paper›PMID 34489413›Full record

ArticleNature communications2021

Nrf1 promotes heart regeneration and repair by regulating proteostasis and redox balance.

Miao Cui, Ayhan Atmanli, Maria Gabriela Morales, Wei Tan, Kenian Chen, Xue Xiao, Lin Xu, Ning Liu, Rhonda Bassel-Duby, Eric N Olson

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
19.5field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
  2. Article
  3. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

21 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Miao CuiDepartment of Molecular Biology, the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Ayhan AtmanliDepartment of Molecular Biology, the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Maria Gabriela MoralesDepartment of Molecular Biology, the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Wei TanDepartment of Molecular Biology, the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Kenian ChenQuantitative Biomedical Research Center, Department of Population & Data Sciences and Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0002-4083-841X
Xue XiaoQuantitative Biomedical Research Center, Department of Population & Data Sciences and Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Lin XuQuantitative Biomedical Research Center, Department of Population & Data Sciences and Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0001-5815-4457
Ning LiuDepartment of Molecular Biology, the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0003-0257-1889
Rhonda Bassel-DubyDepartment of Molecular Biology, the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0001-7568-410X
Eric N OlsonDepartment of Molecular Biology, the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA. eric.olson@utsouthwestern.edu.ORCID 0000-0003-1151-8262
Southwestern Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Training CoreP50HD087351 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI MAMMEN, PRADEEP P.A. · 2020 to 2024
$8.0M
Training CoreU54HD087351 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N · 2015 to 2019
$7.8M
Deciphering the role of a novel micropeptide in cardiac function and dysfunctionR01HL130253 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI BASSEL-DUBY, RHONDA, OLSON, ERIC N · 2016 to 2023
$4.4M
Molecular Dissection of Myoblast Fusion In Muscle Development and RegenerationR01AR067294 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI BASSEL-DUBY, RHONDA, OLSON, ERIC N · 2015 to 2019
$1.8M
Chemically assisted remodeling of infarcted heart tissue by targeting Wnt lipidationR01HL138426 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI BASSEL-DUBY, RHONDA · 2017 to 2020
$1.7M
Dissecting the cytoprotective role of NRF1 in heart regeneration and repairR00HL153683 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CUI, MIAO · 2022 to 2024
$747k
Rodent Ultrasound Imaging SystemS10RR023729 · NCRR · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2009 to 2009
$290k
Dissecting the cytoprotective role of NRF1 in heart regeneration and repairK99HL153683 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI CUI, MIAO · 2021 to 2022
$190k
NCRR NIH HHS S10 RR023729NHLBI NIH HHS K99 HL153683NHLBI NIH HHS R00 HL153683NHLBI NIH HHS R01 HL130253NHLBI NIH HHS R01 HL138426NIAMS NIH HHS R01 AR067294NICHD NIH HHS P50 HD087351NICHD NIH HHS U54 HD087351
6 · The paper itself

Abstract

Following injury, cells in regenerative tissues have the ability to regrow. The mechanisms whereby regenerating cells adapt to injury-induced stress conditions and activate the regenerative program remain to be defined. Here, using the mammalian neonatal heart regeneration model, we show that Nrf1, a stress-responsive transcription factor encoded by the Nuclear Factor Erythroid 2 Like 1 (Nfe2l1) gene, is activated in regenerating cardiomyocytes. Genetic deletion of Nrf1 prevented regenerating cardiomyocytes from activating a transcriptional program required for heart regeneration. Conversely, Nrf1 overexpression protected the adult mouse heart from ischemia/reperfusion (I/R) injury. Nrf1 also protected human induced pluripotent stem cell-derived cardiomyocytes from doxorubicin-induced cardiotoxicity and other cardiotoxins. The protective function of Nrf1 is mediated by a dual stress response mechanism involving activation of the proteasome and redox balance. Our findings reveal that the adaptive stress response mechanism mediated by Nrf1 is required for neonatal heart regeneration and confers cardioprotection in the adult heart.

Indexed as

AnimalsAnimals, NewbornCell DifferentiationDoxorubicinFemaleHeartHeme Oxygenase (Decyclizing)HumansInduced Pluripotent Stem CellsMaleMiceMice, KnockoutMice, TransgenicMyocardial Reperfusion InjuryMyocytes, CardiacNF-E2-Related Factor 1DoxorubicinHeme Oxygenase (Decyclizing)Hmox1 protein, ratNFE2L1 protein, humanNfe2L1 protein, mouseNF-E2-Related Factor 1

Identifiers

PMID34489413
PMCPMC8421386
OpenAlexW3196942636

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.