Evidence map›Paper›PMID 35803125›Full record

ArticleRedox biology2022

Protein palmitoylation-mediated palmitic acid sensing causes blood-testis barrier damage via inducing ER stress.

Xie Ge, Zhaowanyue He, Chun Cao, Tongmin Xue, Jun Jing, Rujun Ma, Wei Zhao, Ling Liu, Kadiliya Jueraitetibaike, Jinzhao Ma and 7 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
7.5field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. The Liver-Testis Axis: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2026
    Review
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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

17 authors at 5 institutions in 1 country.

Xie GeDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Zhaowanyue HeDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Chun CaoThe First School of Clinical Medicine, Southern Medical University, Nanjing, 210002, Jiangsu, China.
Tongmin XueState Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, 210029, Jiangsu, China.
Jun JingDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Rujun MaDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Wei ZhaoDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Ling LiuCAS Center for Excellence in Molecular Cell Sciences, Ministry of Education Key Laboratory for Membrane-less Organelles & Cellular Dynamics, Hefei National Laboratory for Physical Sciences at the Microscale, School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230027, Anhui, China.
Kadiliya JueraitetibaikeDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Jinzhao MaDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Yuming FengDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China; The First School of Clinical Medicine, Southern Medical University, Nanjing, 210002, Jiangsu, China.
Zhang QianDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Zhichuan ZouDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Li ChenDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China.
Chuanhai FuCAS Center for Excellence in Molecular Cell Sciences, Ministry of Education Key Laboratory for Membrane-less Organelles & Cellular Dynamics, Hefei National Laboratory for Physical Sciences at the Microscale, School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230027, Anhui, China. Electronic address: chuanhai@ustc.edu.cn.
Ninghong SongDepartment of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210000, Jiangsu, China. Electronic address: songninghong@126.com.
Bing YaoDepartment of Reproductive Medical Center, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, 210002, Jiangsu, China; State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, 210029, Jiangsu, China. Electronic address: yaobing@nju.edu.cn.
Nanjing General Hospital of Nanjing Military Command · CNUniversity of Science and Technology of China · CNJiangsu Province Hospital · CNNanjing Medical University · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blood-testis barrier (BTB) damage promotes spermatogenesis dysfunction, which is a critical cause of male infertility. Dyslipidemia has been correlated with male infertility, but the major hazardous lipid and the underlying mechanism remains unclear. In this study, we firstly discovered an elevation of palmitic acid (PA) and a decrease of inhibin B in patients with severe dyszoospermia, which leaded us to explore the effects of PA on Sertoli cells. We observed a damage of BTB by PA. PA penetration to endoplasmic reticulum (ER) and its damage to ER structures were exhibited by microimaging and dynamic observation, and consequent ER stress was proved to mediate PA-induced Sertoli cell barrier disruption. Remarkably, we demonstrated a critical role of aberrant protein palmitoylation in PA-induced Sertoli cell barrier dysfunction. An ER protein, Calnexin, was screened out and was demonstrated to participate in this process, and suppression of its palmitoylation showed an ameliorating effect. We also found that ω-3 poly-unsaturated fatty acids down-regulated Calnexin palmitoylation, and alleviated BTB dysfunction. Our results indicate that dysregulated palmitoylation induced by PA plays a pivotal role in BTB disruption and subsequent spermatogenesis dysfunction, suggesting that protein palmitoylation might be therapeutically targetable in male infertility.

Indexed as

Blood-Testis BarrierInfertility, MaleCalnexinHumansLipoylationMalePalmitic AcidSpermatogenesisCalnexinPalmitic AcidBlood-testis barrierEndoplasmic reticulum stressPalmitic acidPalmitoylationSertoli cellTight junction

Identifiers

PMID35803125
PMCPMC9287734
OpenAlexW4283780613

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.