Evidence map›Paper›PMID 41027876›Full record

ArticleSignal transduction and targeted therapy2025

Inhibition of long interspersed nuclear element-1 by nucleoside reverse transcriptase inhibitors attenuates vascular calcification.

Jianshuai Ma, Dayu He, Mingxuan Zhang, Ziting Zhou, Jinkun Cheng, Aoran Huang, Yaxin Lian, Yuncong Shi, Changming Xie, Zhengyan Guan and 4 more

Abstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. The dark genome in cardiovascular medicine.European heart journal · 2026
    Review
  2. 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

14 authors.

Jianshuai MaCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Dayu HeCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Mingxuan ZhangCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Ziting ZhouCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Jinkun ChengCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Aoran HuangCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Yaxin LianCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Yuncong ShiCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Changming XieCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Zhengyan GuanCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Zhengzhipeng ZhangCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Chen XieCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China.
Tingting ZhangCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China. zhangtt73@mail.sysu.edu.cn.
Hui HuangCardiology Department, the Eighth Affiliated Hospital, Joint Laboratory of Guangdong-Hong Kong-Macao Universities for Nutritional Metabolism and Precise Prevention and Control of Major Chronic Diseases, Sun Yat-sen University, Shenzhen, China. huangh8@mail.sysu.edu.cn.ORCID 0000-0001-5716-4012

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82330021, 82270771, 82473913, 82204384, 8247130589, 82400860
6 · The paper itself

Abstract

Vascular calcification (VC) is a critical vascular pathological event, contributing to the rise in both the prevalence and fatality of cardiovascular diseases. However, the lack of effective therapeutic strategies for VC is attributed primarily to the incomplete understanding of its underlying molecular mechanisms. In this study, we discovered that long interspersed nuclear element 1 (LINE1) was significantly upregulated in the calcified arteries of both human individuals and mouse models. Mechanistically, silencing LINE1 expression or inhibiting its activity with adding nucleoside reverse transcriptase inhibitors (NRTIs, a class of validated LINE1 inhibitors) effectively prevented the osteogenic reprogramming of vascular smooth muscle cells (VSMCs). Moreover, NRTIs treatment substantially mitigated VC in chronic kidney disease (CKD)-induced and vitamin D

Indexed as

Long Interspersed Nucleotide ElementsRenal Insufficiency, ChronicReverse Transcriptase InhibitorsVascular CalcificationAnimalsDisease Models, AnimalFemaleHumansMaleMiceMuscle, Smooth, VascularMyocytes, Smooth MuscleSignal TransductionReverse Transcriptase Inhibitors

Identifiers

PMID41027876
PMCPMC12484660

What OpenQuestion holds

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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.