Evidence map›Paper›PMID 28813167›Full record

ArticleAutophagy2017

Lipophagy maintains energy homeostasis in the kidney proximal tubule during prolonged starvation.

Satoshi Minami, Takeshi Yamamoto, Yoshitsugu Takabatake, Atsushi Takahashi, Tomoko Namba, Jun Matsuda, Tomonori Kimura, Jun-Ya Kaimori, Isao Matsui, Takayuki Hamano and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Proximal Tubule-Specific Genetic Deficiency of PPARα Worsens Systemic Lipid and Glucose Metabolism During Fasting.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. MondoA and AKI and AKI-to-CKD Transition.Journal of the American Society of Nephrology : JASN · 2024
    Article
  17. Review
  18. Article
  19. Article
  20. 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

17 authors at 3 institutions in 1 country.

Satoshi Minamia Department of Nephrology , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.
Takeshi Yamamotoa Department of Nephrology , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.
Yoshitsugu Takabatakea Department of Nephrology , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.
Atsushi Takahashia Department of Nephrology , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.
Tomoko Nambaa Department of Nephrology , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.ORCID http://orcid.org/0000-0002-6049-7616
Jun Matsudaa Department of Nephrology , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.
Tomonori Kimuraa Department of Nephrology , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.
Jun-Ya Kaimorib Department of Advanced Technology for Transplantation , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.
Isao Matsuia Department of Nephrology , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.ORCID http://orcid.org/0000-0001-8378-6130
Takayuki Hamanoc Department of Comprehensive Kidney Disease Research (CKDR) , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.
Hiroaki Takedad Division of Metabolomics, Medical Institute of Bioregulation , Kyushu University , Higashi-ku , Fukuoka , Japan.
Masatomo Takahashid Division of Metabolomics, Medical Institute of Bioregulation , Kyushu University , Higashi-ku , Fukuoka , Japan.
Yoshihiro Izumid Division of Metabolomics, Medical Institute of Bioregulation , Kyushu University , Higashi-ku , Fukuoka , Japan.
Takeshi Bambad Division of Metabolomics, Medical Institute of Bioregulation , Kyushu University , Higashi-ku , Fukuoka , Japan.
Taiji Matsusakae Institute of Medical Sciences and Department of Molecular Life Sciences , Tokai University School of Medicine , Isehara , Kanagawa , Japan.
Fumio Niimuraf Department of Pediatrics , Tokai University School of Medicine , Isehara , Kanagawa , Japan.
Yoshitaka Isakaa Department of Nephrology , Osaka University Graduate School of Medicine , Suita , Osaka , Japan.
The University of Osaka · JPKyushu University · JPTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy is a self-degradation process that combats starvation. Lipids are the main energy source in kidney proximal tubular cells (PTCs). During starvation, PTCs increase fatty acid (FA) uptake, form intracellular lipid droplets (LDs), and hydrolyze them for use. The involvement of autophagy in lipid metabolism in the kidney remains largely unknown. Here, we investigated the autophagy-mediated regulation of renal lipid metabolism during prolonged starvation using PTC-specific Atg5-deficient (atg5-TSKO) mice and an in vitro serum starvation model. Twenty-four h of starvation comparably induced LD formation in the PTCs of control and atg5-TSKO mice; however, additional 24 h of starvation reduced the number of LDs in control mice, whereas increases were observed in atg5-TSKO mice. Autophagic degradation of LDs (lipophagy) in PTCs was demonstrated by electron microscopic observation and biochemical analysis. In vitro pulse-chase assays demonstrated that lipophagy mobilizes FAs from LDs to mitochondria during starvation, whereas impaired LD degradation in autophagy-deficient PTCs led to decreased ATP production and subsequent cell death. In contrast to the in vitro assay, despite impaired LD degradation, kidney ATP content was preserved in 48-h starved atg5-TSKO mice, probably due to increased utilization of ketone bodies. This compensatory mechanism was accompanied by a higher plasma FGF21 (fibroblast growth factor 21) level and its expression in the PTCs; however, this was not essential for the production of ketone bodies in the liver during prolonged starvation. In conclusion, lipophagy combats prolonged starvation in PTCs to avoid cellular energy depletion.

Indexed as

AnimalsAutophagyAutophagy-Related Protein 5Biological TransportCells, CulturedHomeostasisKidney Tubules, ProximalLipid DropletsLipid MetabolismLipolysisMiceMice, Inbred C57BLMice, KnockoutStarvationAtg5 protein, mouseAutophagy-Related Protein 5autophagic fluxautophagylipid dropletlipophagylysosomemitochondriaβ-oxidation

Identifiers

PMID28813167
PMCPMC5640178
OpenAlexW2745545503

What OpenQuestion holds

Textmetadata
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.