Evidence map›Paper›PMID 32106109›Full record

ArticleThe Journal of clinical investigation2020

Salt-inducible kinase 1 maintains HDAC7 stability to promote pathologic cardiac remodeling.

Austin Hsu, Qiming Duan, Sarah McMahon, Yu Huang, Sarah Ab Wood, Nathanael S Gray, Biao Wang, Benoit G Bruneau, Saptarsi M Haldar

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Histone Deacetylase 7 protects against pathologic cardiac hypertrophy.Journal of molecular and cellular cardiology · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Salt and Gut Microbiota in Heart Failure.Current hypertension reports · 2023
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Austin HsuBiomedical Sciences Graduate Program, UCSF, San Francisco, California, USA.
Qiming DuanRoddenberry Center for Stem Cell Biology and Medicine, Gladstone Institutes, San Francisco, California, USA.
Sarah McMahonBiomedical Sciences Graduate Program, UCSF, San Francisco, California, USA.
Yu HuangRoddenberry Center for Stem Cell Biology and Medicine, Gladstone Institutes, San Francisco, California, USA.
Sarah Ab WoodGladstone Institutes, San Francisco, California, USA.
Nathanael S GrayDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Biao WangCardiovascular Research Institute.
Benoit G BruneauGladstone Institutes, San Francisco, California, USA.
Saptarsi M HaldarRoddenberry Center for Stem Cell Biology and Medicine, Gladstone Institutes, San Francisco, California, USA.
Gladstone Institutes · USCardiovascular Institute Hospital · JPHarvard University · US

Funding

Regulation of Chromatin Signaling in Heart Failure by the BRD4 Bromodomain Protein.R01HL127240 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY, SRIVASTAVA, DEEPAK · 2015 to 2022
$6.4M
PREDOCTORAL TRAINING IN BIOMEDICAL SCIENCEST32GM008568 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANSEL, KARL MARK · 1995 to 2019
$6.3M
EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR018928 · NCRR · J. DAVID GLADSTONE INSTITUTES · PI MAHLEY, ROBERT W. · 2003 to 2003
$2.1M
Transcriptional control in brown and beige adipocytesR01DK105175 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WANG, BIAO · 2015 to 2019
$1.8M
NCRR NIH HHS C06 RR018928NHLBI NIH HHS R01 HL127240NIDDK NIH HHS R01 DK105175NIGMS NIH HHS T32 GM008568
6 · The paper itself

Abstract

Salt-inducible kinases (SIKs) are key regulators of cellular metabolism and growth, but their role in cardiomyocyte plasticity and heart failure pathogenesis remains unknown. Here, we showed that loss of SIK1 kinase activity protected against adverse cardiac remodeling and heart failure pathogenesis in rodent models and cardiomyocytes derived from human induced pluripotent stem cells. We found that SIK1 phosphorylated and stabilized histone deacetylase 7 (HDAC7) protein during cardiac stress, an event that is required for pathologic cardiomyocyte remodeling. Gain- and loss-of-function studies of HDAC7 in cultured cardiomyocytes implicated HDAC7 as a prohypertrophic signaling effector that can induce c-Myc expression, indicating a functional departure from the canonical MEF2 corepressor function of class IIa HDACs. Taken together, our findings reveal what we believe to be a previously unrecognized role for a SIK1/HDAC7 axis in regulating cardiac stress responses and implicate this pathway as a potential target in human heart failure.

Indexed as

Ventricular RemodelingAnimalsHistone DeacetylasesHumansMiceMyocytes, CardiacPhosphorylationProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyHdac7 protein, mouseHDAC7 protein, ratHistone DeacetylasesProtein Serine-Threonine KinasesSik1 protein, mouseSik1 protein, ratCardiologyCardiovascular diseaseHeart failureMuscle BiologySignal transduction

Identifiers

PMID32106109
PMCPMC7259992
OpenAlexW3008274390

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.