Evidence map›Paper›PMID 35728063›Full record

ArticleBlood advances2022

CPT2 K79 acetylation regulates platelet life span.

Xuemei Fan, Yang Wang, Xiaohong Cai, Yingzhi Shen, Tongran Xu, Yanyan Xu, Jinke Cheng, Xuefeng Wang, Lin Zhang, Jing Dai and 2 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Dysfunctional glycolysis-UCP2-fatty acid oxidation promotes CTLA4Molecular medicine (Cambridge, Mass.) · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025
    Review
  13. Article
  14. Article
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

12 authors at 2 institutions in 1 country.

Xuemei FanDepartment of Biochemistry and Molecular Cell Biology, and.ORCID 0000-0001-7380-2408
Yang WangDepartment of Biochemistry and Molecular Cell Biology, and.
Xiaohong CaiDepartment of Blood Transfusion, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yingzhi ShenDepartment of Biochemistry and Molecular Cell Biology, and.
Tongran XuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian, China; and.
Yanyan XuDepartment of Biochemistry and Molecular Cell Biology, and.
Jinke ChengDepartment of Biochemistry and Molecular Cell Biology, and.ORCID 0000-0002-4344-5363
Xuefeng WangDepartment of Laboratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lin ZhangDepartment of Biochemistry and Molecular Cell Biology, and.
Jing DaiDepartment of Laboratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shuhai LinState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian, China; and.ORCID 0000-0002-4782-5320
Junling LiuDepartment of Biochemistry and Molecular Cell Biology, and.ORCID 0000-0002-2510-790X
Shanghai Jiao Tong University · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The short life span of platelets is a major challenge to platelet transfusion services because of the lack of effective intervention. Here, we found that the accumulation of long-chain acylcarnitines (LCACs) is responsible for mitochondrial damage and platelet storage lesion. Further studies showed that the blockade of fatty acid oxidation and the activation of AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase/carnitine palmitoyltransferase 1 (CPT1) pathways that promote fatty acid metabolism are important reasons for the accumulation of LCACs. The excessive accumulation of LCACs can cause mitochondrial damage and a short life span of stored platelets. The mechanism study elucidated that NAD+ exhaustion and the subsequent decrease in sirtuin 3 (Sirt3) activity caused an increase in the level of CPT2 K79 acetylation, which is the primary cause of the blockade of fatty acid oxidation and the accumulation of LCACs. Blocking LCAC generation with the inhibitors of AMPK or CPT1, the agonists of Sirt3, and antioxidants tremendously retarded platelet storage lesion in vitro and prolonged the survival of stored platelets in vivo posttransfusion with single or combined use. In summary, we discovered that CPT2 acetylation attenuates fatty acid oxidation and exacerbates platelet storage lesion and may serve as a new target for improving platelet storage quality.

Indexed as

Sirtuin 3AcetylationAMP-Activated Protein KinasesCarnitine O-PalmitoyltransferaseFatty AcidsLongevityAMP-Activated Protein KinasesCarnitine O-PalmitoyltransferaseFatty AcidsSirtuin 3

Identifiers

PMID35728063
PMCPMC9631617
OpenAlexW4283206164

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.