Evidence map›Paper›PMID 42560989›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026

PKA-Mediated Proteasome Activation Protects Against Cardiac Remodeling and Heart Failure During Systolic Overload.

Md Salim Ahammed, Penglong Wu, Yifan Wang, Liuqing Yang, Jack O Sternburg, Faqian Li, Jinbao Liu, Xuejun Wang

Abstract read
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In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Md Salim AhammedDivision of Biomedical and Translational Sciences, University of South Dakota Sanford School of Medicine, Vermillion, South Dakota, USA.
Penglong WuDivision of Biomedical and Translational Sciences, University of South Dakota Sanford School of Medicine, Vermillion, South Dakota, USA.
Yifan WangDivision of Biomedical and Translational Sciences, University of South Dakota Sanford School of Medicine, Vermillion, South Dakota, USA.
Liuqing YangDivision of Biomedical and Translational Sciences, University of South Dakota Sanford School of Medicine, Vermillion, South Dakota, USA.
Jack O SternburgDivision of Biomedical and Translational Sciences, University of South Dakota Sanford School of Medicine, Vermillion, South Dakota, USA.
Faqian LiDepartment of Pathology and Laboratory Medicine, Joe R. and Teresa Lozano Long School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Jinbao LiuGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0003-2220-2407
Xuejun WangDivision of Biomedical and Translational Sciences, University of South Dakota Sanford School of Medicine, Vermillion, South Dakota, USA.ORCID https://orcid.org/0000-0001-9267-1343

Funding

Ubiquitin receptors and cardiac proteotoxicityR01HL072166 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2003 to 2023
$6.9M
Cardiac Pathophysiology of Proteasome PhosphoregulationR01HL153614 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI XUEJUN WANG · 2020 to 2026
$2.9M
Priming the proteasome to protect against aging and Alzheimer's diseaseR01AG072510 · NIA · UNIVERSITY OF SOUTH DAKOTA · PI XUEJUN WANG, Hongmin Wang · 2025 to 2026
$1.0M
HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL072166HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL153614HHS | NIH | National Institute on Aging (NIA) R01AG072510NHLBI NIH HHS R01 HL072166NHLBI NIH HHS R01 HL153614NIA NIH HHS R01 AG072510
6 · The paper itself

Abstract

Heart failure (HF) resulting from chronic systolic overload is associated with increased burden on proteostasis and impaired proteasome function. Phosphorylation of proteasome subunit RPN6/PSMD11 at Ser14 (pS14-RPN6) mediates the activation of 26S proteasomes by PKA, but its significance in common forms of heart disease remains obscure. Hence, we investigated the impact of genetic blockade of pS14-RPN6 on cardiac remodeling and HF during systolic overload, a common condition occurring in hypertension and aortic stenosis. We detected marked increases in ubiquitin conjugates, along with elevated levels of RPN6 and pS14-RPN6 proteins in myocardial tissues from human patients with nonischemic HF. Similarly, myocardial pS14-Rpn6 was increased in wild-type mice 2 and 4 weeks after transverse aortic constriction (TAC). Compared with wild-type littermates, mice with genetic blockade of pS14-Rpn6 resulting from germline knock-in of Rpn6

Indexed as

Cyclic AMP-Dependent Protein KinasesHeart FailureProteasome Endopeptidase ComplexVentricular RemodelingAnimalsHumansMaleMiceMice, Inbred C57BLMyocardiumPhosphorylationCyclic AMP-Dependent Protein KinasesProteasome Endopeptidase ComplexcAMP‐dependent kinasecardiac hypertrophyheart failureproteasome phosphorylationproteostasisRPN6/PSMD11systolic overload

Identifiers

PMID42560989
PMCPMC13446592

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LicenceCC BY-NC-ND
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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.