PXD067998

PXD067998 is an original dataset announced via ProteomeXchange.

Title	Propionylation at OXCT1 lysine-296 is the key mechanism of atrial fibrillation in both patients and atrial-specific knockout of the LKB1 mouse model
Description	Atrial fibrillation (AF), the most prevalent clinical arrhythmia, imposes a major global health burden through elevated risks of stroke, heart failure, and mortality. Lysine propionylation (Kpr) is mainly involved in metabolic regulation and plays an important role in cardiac pathophysiology. However, the specific role and mechanism of Kpr in AF remain unclear. Here we show that significantly increased Kpr levels of 3-oxoacid CoA-transferase 1 (OXCT1) at lysine-296 (K296) were found both in atrial tissues of AF mice induced by atrial-specific LKB1 knockout and in right atrial tissues of patients with postoperative AF (POAF) after coronary artery bypass grafting (CABG). We found that propionylation greatly reduced the enzyme activity of OXCT1 and inhibited its interaction with acetyl-CoA acetyltransferase 1 (ACAT1), leading to decreased ACAT1 protein expression. Furthermore, on the one hand, these changes reduced the production of succinate and adenosine triphosphate (ATP), resulting in an imbalance of mitochondrial energy metabolism, and on the other hand, increased the production of intracellular ROS and mitochondrial ROS (mitoROS), triggering oxidative stress. Our results reveal that elevated propionylation of OXCT1 at K296 is a crucial molecular mechanism underlying AF, providing new insights into the etiology of AF and potential therapeutic targets.
HostingRepository	PRIDE
AnnounceDate	2026-08-07
AnnouncementXML	Submission_2026-08-06_23:15:00.722.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Hai-Tao Hou
SpeciesList	scientific name: Homo sapiens (Human); NCBI TaxID: NEWT:9606; scientific name: Mus musculus (Mouse); NCBI TaxID: NEWT:10090;
ModificationList	propanoylated residue
Instrument	timsTOF HT

Revision	Datetime	Status	ChangeLog Entry
0	2025-09-02 07:19:21	ID requested
⏵ 1	2026-08-06 23:15:01	announced

Dataset with its publication pending

submitter keyword: Atrial fibrillation, LKB1, OXCT1, oxidative stress, Protein post-translational modifications, Propionylation

HOU HT
contact affiliation	TEDA International Cardiovascular Hospital
contact email	hhtpk007@163.com
lab head
Hai-Tao Hou
contact affiliation	Teda International Cardiovascular Hospital
contact email	hhtpk007@163.com
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD067998
     1. Label: PRIDE project
     2. Name: Propionylation at OXCT1 lysine-296 is the key mechanism of atrial fibrillation in both patients and atrial-specific knockout of the LKB1 mouse model