Evidence mapPaperPMID 39896343Full record

ArticleNon-coding RNA research2025

Inhibition of MALAT1 facilitates ROS accumulation via the Keap1/HO-1 pathway to enhance photodynamic therapy in secondary hyperparathyroidism.

Ying Wen, Yitong Li, Danhua Zhang, Ziru Liu, Hong Liu, Xiejia Li, Wei Wu, Liyun Zeng, Qiongyan Zou, Wenjun Yi

Abstract read
In one paragraph

Article in Non-coding RNA research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
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

10 authors.

Ying WenDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Clinical Research Center for Breast Disease in Hunan Province, Changsha, Hunan, 410011, China.
Yitong LiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Clinical Research Center for Breast Disease in Hunan Province, Changsha, Hunan, 410011, China.
Danhua ZhangDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Clinical Research Center for Breast Disease in Hunan Province, Changsha, Hunan, 410011, China.
Ziru LiuDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Clinical Research Center for Breast Disease in Hunan Province, Changsha, Hunan, 410011, China.
Hong LiuDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Xiejia LiDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Wei WuDepartment of General Surgery, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, China.
Liyun ZengDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Clinical Research Center for Breast Disease in Hunan Province, Changsha, Hunan, 410011, China.
Qiongyan ZouDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Clinical Research Center for Breast Disease in Hunan Province, Changsha, Hunan, 410011, China.
Wenjun YiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Clinical Research Center for Breast Disease in Hunan Province, Changsha, Hunan, 410011, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The prevalence of secondary hyperparathyroidism (SHPT) in advanced chronic kidney disease (CKD) exceeds 80 %. Our previous study indicated that photodynamic therapy (PDT) has potential for treating SHPT. Long noncoding RNA (lncRNA) is involved in various oxidative stress and apoptotic processes, but the molecular mechanism remains unreported. In this study, we found that PDT induced apoptosis in SHPT through reactive oxygen species (ROS) accumulation. The expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and heme oxygenase 1 (HO-1) within SHPT was upregulated after PDT. Inhibition of MALAT1 increased PDT-induced ROS, which promoted the apoptosis. Pearson correlation analysis confirmed that there was a positive correlation between MALAT1 and HO-1, and MALAT1 inhibition down-regulated HO-1, whereas concomitant overexpression of HO-1 was able to eliminate the PDT-induced ROS and inhibit apoptosis. The direct binding of MALAT1 to Kelch-like ECH-associated protein 1 (Keap1) protein was confirmed by high-throughput sequencing, RNA pulldown, silver staining and western blotting assays. Si-Keap1 was able to rescue the down-regulation of HO-1 caused by MALAT1 inhibition, restoring the elimination of ROS by HO-1 and attenuating the effect of PDT. In addition, PDT effectively reduced parathyroid hormone (PTH) secretion in SHPT rats, and this effect was further enhanced in combination with MALAT1 inhibitors. Overall, MALAT1 activates downstream HO-1 expression by binding to Keap1, thereby reducing ROS and inhibiting apoptosis, which in turn mediates PDT resistance in SHPT. Inhibition of MALAT1 significantly enhanced the efficacy of PDT, suggesting a potential therapeutic target for improving PDT for SHPT outcomes.

Indexed as

Long chain non-coding RNAPhotodynamic therapyReactive oxygen speciesSecondary hyperparathyroidism

Identifiers

PMID39896343
PMCPMC11787669

What Socratic holds

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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 Socratic graph.