Evidence map›Paper›PMID 42874129›Full record

ArticleRedox biology2026

HDAC1-mediated SUCLA2 lysine β-hydroxybutyrylation modulates myocardial mitochondrial function in sepsis-induced heart dysfunction.

Ri Wen, Wanshan Ning, Xin-Mei Huang, Peng-Hui Hao, Jingjing Yang, Wei Liu, Yu-Hang Yang, Chun-Feng Liu, Ni Yang, Yaping Guo and 1 more

Abstract read
In one paragraph

Article in Redox 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.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

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No citing paper in PubMed yet.

4 · The record

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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.

Ri WenDepartment of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
Wanshan NingInstitute for Clinical Medical Research, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China.
Xin-Mei HuangDepartment of Endocrinology, Shanghai Fifth People's Hospital, Fudan University, Shanghai, 200240, China.
Peng-Hui HaoDepartment of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
Jingjing YangDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361003, China.
Wei LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Yu-Hang YangDepartment of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
Chun-Feng LiuDepartment of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
Ni YangDepartment of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, 110004, China. Electronic address: yangni616@hotmail.com.
Yaping GuoDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China. Electronic address: guoyaping@zzu.edu.cn.
Tie-Ning ZhangDepartment of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, 110004, China. Electronic address: cmuztn@vip.qq.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLysine β-hydroxybutyrylation (Kbhb) is associated with energy regulation and mitochondrial function, and its role in sepsis-induced heart dysfunction has not been elucidated.

objectivesReveals the extensive effects of Kbhb in sepsis-induced heart dysfunction and identifies the potential targets.

methodsA septic heart dysfunction rat model was induced by lipopolysaccharide intraperitoneal injection. Proteomic and β-hydroxybutyrylomic analyses were conducted to assess alterations in Kbhb between cardiac tissues from the control and lipopolysaccharide rats. Putative regulatory proteins were identified by leveraging a multifaceted hybrid learning framework combined with protein language models. Lysine to arginine (R) mutation was made to mimic decreased Kbhb levels. Transcriptomic analysis was further performed to predict the potential downstream mechanisms.

resultsSuccinate-CoA Ligase ADP-Forming Subunit Beta (SUCLA2) was selected because of its role in mitochondrial function, and the Kbhb level at the K444 site was significantly different. Decreased Kbhb level at K444 of SUCLA2 was confirmed in septic cardiac tissues and lipopolysaccharide-treated H9c2 cardiomyocytes using specific antibody. SUCLA2

conclusionsReduced SUCLA2 Kbhb level at K444 site aggravates myocardial mitochondrial dysfunction, leading to sepsis-induced heart dysfunction. This study reveals a novel function of Kbhb in sepsis-induced heart dysfunction and elucidates the mechanism of SUCLA2 K444 Kbhb.

Indexed as

Histone deacetylase 1Lysine β-hydroxybutyrylationMitochondrial functionSepsis-induced heart dysfunctionSuccinate-CoA ligase ADP-Forming subunit beta

Identifiers

PMID42874129
PMCPMC13683460

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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.