Evidence map›Paper›PMID 34630132›Full record

ArticleFrontiers in physiology2021

A-Lipoic Acid Alleviates Folic Acid-Induced Renal Damage Through Inhibition of Ferroptosis.

Xue Li, Yu Zou, Yuan-Yuan Fu, Jia Xing, Kai-Yue Wang, Peng-Zhi Wan, Xiao-Yue Zhai

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
7.1field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Ferroptosis inhibitors: mechanisms of action and therapeutic potential.Cellular and molecular life sciences : CMLS · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
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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

7 authors at 1 institution in 1 country.

Xue LiDepartment of Histology and Embryology, Basic Medical College, China Medical University, Shenyang, China.
Yu ZouDepartment of Histology and Embryology, Basic Medical College, China Medical University, Shenyang, China.
Yuan-Yuan FuDepartment of Histology and Embryology, Basic Medical College, China Medical University, Shenyang, China.
Jia XingDepartment of Histology and Embryology, Basic Medical College, China Medical University, Shenyang, China.
Kai-Yue WangDepartment of Histology and Embryology, Basic Medical College, China Medical University, Shenyang, China.
Peng-Zhi WanDepartment of Nephrology, First Affiliated Hospital of China Medical University, Shenyang, China.
Xiao-Yue ZhaiDepartment of Histology and Embryology, Basic Medical College, China Medical University, Shenyang, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Folic acid (FA)-induced acute kidney injury (AKI) is characterized by the disturbance of redox homeostasis, resulting in massive tubular necrosis and inflammation. Α-lipoic acid (LA), as an antioxidant, has been reported to play an important role in renal protection, but the underlying mechanism remains poorly explored. The aim of this study is to investigate the protective effect of LA on FA-induced renal damage. Our findings showed that LA could ameliorate renal dysfunction and histopathologic damage induced by FA overdose injection. Moreover, FA injection induced severe inflammation, indicated by increased release of pro-inflammatory cytokines tumor necrosis factor (TNF)-α and IL-1β, as well as infiltration of macrophage, which can be alleviated by LA supplementation. In addition, LA not only reduced the cellular iron overload by upregulating the expressions of Ferritin and ferroportin (FPN), but also mitigated reactive oxygen species (ROS) accumulation and lipid peroxidation by increasing the levels of antioxidant glutathione (GSH) and glutathione peroxidase-4 (GPX4). More importantly, we found that LA supplementation could reduce the number of Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive tubular cells caused by FA, indicating that the tubular cell death mediated by ferroptosis may be inhibited. Further study demonstrated that LA supplementation could reverse the decreased expression of cystine/glutamate antiporter xCT (SLC7A11), which mediated GSH synthesis. What is more, mechanistic study indicated that p53 activation was involved in the inhibitory effect of SLC7A11 induced by FA administration, which could be suppressed by LA supplementation. Taken together, our findings indicated that LA played the protective effect on FA-induced renal damage mainly by inhibiting ferroptosis.

Indexed as

A-lipoic acidferroptosisfolic acidp53renal damage

Identifiers

PMID34630132
PMCPMC8493959
OpenAlexW3200609399

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.