Evidence map›Paper›PMID 33767132›Full record

ArticleCell death & disease2021

The critical role of FXR is associated with the regulation of autophagy and apoptosis in the progression of AKI to CKD.

Dong-Hyun Kim, Jung Sun Park, Hoon-In Choi, Chang Seong Kim, Eun Hui Bae, Seong Kwon Ma, Soo Wan Kim

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
6.3field-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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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  16. Intestinal epithelial autophagy is required for the regenerative benefit of calorie restriction.American journal of physiology. Gastrointestinal and liver physiology · 2023
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  19. Role of FXR in Renal Physiology and Kidney Diseases.International journal of molecular sciences · 2023
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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.

Dong-Hyun KimDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.ORCID 0000-0001-8995-9426
Jung Sun ParkDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Hoon-In ChoiDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Chang Seong KimDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Eun Hui BaeDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Seong Kwon MaDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Soo Wan KimDepartment of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea. skimw@chonnam.ac.kr.
Chonnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is important for cells to break down and recycle cellular proteins, remove damaged organelles, and especially, for recovery from acute kidney injury (AKI). Despite research on the role and cellular mechanism of autophagy in AKI, the role of autophagy in the progression to chronic kidney disease (CKD) remains poorly understood. Here, using farnesoid X receptor (FXR) knockout (KO) mice, we determined whether FXR prevents the progression of AKI to CKD after renal ischemic-reperfusion (such as I/R) injury through the regulation of renal autophagy and apoptosis. FXR regulated genes that participate in renal autophagy under feeding and fasting conditions, such as hepatic autophagy, and the activation of FXR by agonists, such as GW4064 and INT-747, attenuated the increased autophagy and apoptosis of hypoxia-induced human renal proximal tubule epithelial (HK2) cells. The expression levels of autophagy-related and apoptosis-related proteins in FXR KO mice were increased compared with those in wild-type (WT) mice. We also showed that the increase in reactive oxidative species (ROS) in hypoxia-treated HK2 cells was attenuated by treatment with FXR agonist or by FXR overexpression, and that the level of ROS was elevated in FXR-deficient cells and mice. At 28 days after I/R injury, the autophagy levels were still elevated in FXR KO mice, and the expression levels of fibrosis-related proteins and ROS deposits were higher than those in WT mice. In conclusion, the regulation of renal autophagy and apoptosis by FXR may be a therapeutic target for the early stages of kidney damage, and the progression of AKI to CKD.

Indexed as

Acute Kidney InjuryAnimalsApoptosisAutophagyCell LineDisease ProgressionEpithelial CellsHumansKidney Tubules, ProximalMaleMiceMice, Inbred C57BLMice, KnockoutReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRenal Insufficiency, ChronicReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and Nuclear

Identifiers

PMID33767132
PMCPMC7994637
OpenAlexW3137314888

What OpenQuestion holds

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LicenceCC BY
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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.