Evidence map›Paper›PMID 37057309›Full record

ArticleCell proliferation2023

LRH-1 activation alleviates diabetes-induced podocyte injury by promoting GLS2-mediated glutaminolysis.

Jijia Hu, Zongwei Zhang, Hongtu Hu, Keju Yang, Zijing Zhu, Qian Yang, Wei Liang

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026
    Review
  8. Article
  9. The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Glutaminolysis is a Potential Therapeutic Target for Kidney Diseases.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  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

7 authors at 2 institutions in 1 country.

Jijia HuDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.ORCID https://orcid.org/0000-0002-8847-845X
Zongwei ZhangDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Hongtu HuDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Keju YangDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Zijing ZhuDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Qian YangDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Wei LiangDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Wuhan University · CNChina Three Gorges University · CN

Funding

National Natural Science Foundation of China 8197063Natural Science Foundation of Hubei Province 2022CFB667
6 · The paper itself

Abstract

Alteration of metabolic phenotype in podocytes directly contributes to the development of albuminuria and renal injury in conditions of diabetic kidney disease (DKD). This study aimed to identify and evaluate liver receptor homologue-1 (LRH-1) as a possible therapeutic target that alleviates glutamine (Gln) metabolism disorders and mitigates podocyte injury in DKD. Metabolomic and transcriptomic analyses were performed to characterize amino acid metabolism changes in the glomeruli of diabetic mice. Next, Western blotting, immunohistochemistry assays, and immunofluorescence staining were used to detect the expression of different genes in vitro and in vivo. Furthermore, Gln and glutamate (Glu) content as well as ATP generation were examined. A decrease in LRH-1 and glutaminase 2 (GLS2) expression was detected in diabetic podocytes. Conversely, the administration of LRH-1 agonist (DLPC) upregulated the expression of GLS2 and promoted glutaminolysis, with an improvement in mitochondrial dysfunction and less apoptosis in podocytes compared to those in vehicle-treated db/db mice. Our study indicates the essential role of LRH-1 in governing the Gln metabolism of podocytes, targeting LRH-1 could restore podocytes from diabetes-induced disturbed glutaminolysis in mitochondria.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NephropathiesPodocytesAnimalsGlutaminaseKidneyKidney GlomerulusMiceReceptors, Cytoplasmic and NuclearGls2 protein, mouseGlutaminaseNr5a2 protein, mouseReceptors, Cytoplasmic and Nuclear

Identifiers

PMID37057309
PMCPMC10623971
OpenAlexW4365478835

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.