Evidence map›Paper›PMID 31714893›Full record

ArticleAging2019

Promising therapeutic effect of thapsigargin nanoparticles on chronic kidney disease through the activation of Nrf2 and FoxO1.

Fong-Yu Cheng, Yu-Hsuan Lee, Yung-Ho Hsu, I-Jen Chiu, Yu-Jhe Chiu, Yuh-Feng Lin, Hui-Wen Chiu

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Nanoparticles in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026
    Review
  3. Nanotherapeutics in Kidney Disease: Innovations, Challenges, and Future Directions.Journal of the American Society of Nephrology : JASN · 2025
    Review
  4. Review
  5. Review
  6. The Role of Cyclodextrins in COVID-19 Therapy-A Literature Review.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Review
  9. GlutathioneThe Journal of pharmacology and experimental therapeutics · 2021
    Article
  10. Article
  11. Review
  12. 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 4 institutions in 1 country.

Fong-Yu ChengDepartment of Chemistry, Chinese Culture University, Taipei, Taiwan.
Yu-Hsuan LeeDepartment of Cosmeceutics, China Medical University, Taichung, Taiwan.
Yung-Ho HsuDivision of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
I-Jen ChiuDivision of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Yu-Jhe ChiuDivision of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Yuh-Feng LinDivision of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Hui-Wen ChiuDivision of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Taipei Medical University-Shuang Ho Hospital · TWTaipei Medical University · TWChina Medical University · TWChinese Culture University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathophysiological states cause misfolded protein accumulation in the endoplasmic reticulum (ER). Then, ER stress and the unfolded protein response (UPR) are activated. Targeting ER stress may enhance the adaptive UPR and then protect the cell against pathogenic environments. In the present study, we utilized nanotechnology to synthesize thapsigargin nanoparticles (TG NPs) which induced ER stress and the UPR pathway, to study the role of ER stress and autophagy in chronic kidney disease (CKD). We found that the mRNA levels of ER stress- and autophagy-related molecules were elevated in the renal tissue of CKD patients compared to those of healthy individuals. Furthermore, TG NPs induced the UPR pathway and autophagy in HK-2 human kidney tubular epithelial cells. TG NPs protected HK-2 cells against oxidative stress-induced cell death through the activation of Nrf2 and FoxO1. The siRNA-mediated inhibition of Nrf2 or FoxO1 resulted in enhanced oxidative stress-induced cytotoxicity in HK-2 cells. In a mouse model of adenine diet-induced CKD, TG NPs and KIM-1-TG NPs ameliorated renal injury through the stimulation of ER stress and its downstream pathways. Our findings suggest that the induction of ER stress using pharmacological agents may offer a promising therapeutic strategy for preventing or interfering with CKD progression.

Indexed as

AdenineAnimalsAutophagyCell LineDrug Evaluation, PreclinicalEndoplasmic Reticulum StressForkhead Box Protein O1HumansMaleMiceMice, Inbred C57BLNanoparticlesNF-E2-Related Factor 2Renal Insufficiency, ChronicThapsigarginAdenineForkhead Box Protein O1Foxo1 protein, mouseNfe2l2 protein, mouseNF-E2-Related Factor 2Thapsigarginautophagychronic kidney diseaseendoplasmic reticulum stressFoxO1Nrf2

Identifiers

PMID31714893
PMCPMC6874456
OpenAlexW2989110083

What OpenQuestion 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 OpenQuestion graph.