Evidence map›Paper›PMID 35127371›Full record

ReviewActa pharmaceutica Sinica. B2022

Therapeutic regulation of autophagy in hepatic metabolism.

Katherine Byrnes, Sophia Blessinger, Niani Tiaye Bailey, Russell Scaife, Gang Liu, Bilon Khambu

Open access · diamondAbstract readReview
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 124 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Contradictory Effects on Hepatocytes in ASMD.International journal of molecular sciences · 2026
    Review
  7. Article
  8. Review
  9. Article
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  11. Article
  12. Review
  13. Article
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  15. Review
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  18. Article
  19. Implications of host sex on liver metabolism duringFrontiers in cellular and infection microbiology · 2026
    Review
  20. Article

27 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Katherine ByrnesDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Sophia BlessingerDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Niani Tiaye BaileyDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Russell ScaifeDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Gang LiuDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Bilon KhambuDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Tulane University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic homeostasis requires dynamic catabolic and anabolic processes. Autophagy, an intracellular lysosomal degradative pathway, can rewire cellular metabolism linking catabolic to anabolic processes and thus sustain homeostasis. This is especially relevant in the liver, a key metabolic organ that governs body energy metabolism. Autophagy's role in hepatic energy regulation has just begun to emerge and autophagy seems to have a much broader impact than what has been appreciated in the field. Though classically known for selective or bulk degradation of cellular components or energy-dense macromolecules, emerging evidence indicates autophagy selectively regulates various signaling proteins to directly impact the expression levels of metabolic enzymes or their upstream regulators. Hence, we review three specific mechanisms by which autophagy can regulate metabolism: A) nutrient regeneration, B) quality control of organelles, and C) signaling protein regulation. The plasticity of the autophagic function is unraveling a new therapeutic approach. Thus, we will also discuss the potential translation of promising preclinical data on autophagy modulation into therapeutic strategies that can be used in the clinic to treat common metabolic disorders.

Indexed as

AIM, Atf8 interacting motifATGL, adipose triglyceride lipaseATL3, Atlastin GTPase 3ATM, ATM serine/threonine kinaseAutophagyBA, bile acidBCL2L13, BCL2 like 13BNIP3, BCL2 interacting protein 3BNIP3L, BCL2 interacting protein 3 likeCAR, constitutive androstane receptorCCPG1, cell cycle progression 1CLN3, lysosomal/endosomal transmembrane proteinCMA, chaperonin mediated autophagyCREB, cAMP response element binding proteinCRY1, cryptochrome 1Cryptochrome 1CYP27A1, sterol 27-hydroxylaseCYP7A1, cholesterol 7α-hydroxylaseDFCP1, double FYVE-containing protein 1FAM134B, family with sequence similarity 134, member BFarnesoid X receptorFFA, free fatty acidFOXO1, Forkhead box O1FUNDC1, FUN14 domain containing 1FXR, farnesoid X receptorGABARAPL1, GABA type A receptor associated protein like 1GIM, GABARAP-interacting motifLAAT-1, lysosomal amino acid transporter 1 homologueLALP70, lysosomal apyrase-like protein of 70 kDaLAMP1, lysosomal-associated membrane protein-1LAMP2, lysosomal-associated membrane protein-2LD, lipid dropletLIMP1, lysosomal integral membrane protein-1LIMP3, lysosomal integral membrane protein-3LIR, LC3 interacting regionLiver metabolismLXRa, liver X receptor aLYAAT-1, lysosomal amino acid transporter 1LysosomeMCOLN1, mucolipin 1MFSD1, major facilitator superfamily domain containing 1mTORC1, mammalian target of rapamycin complex 1NAFLD, non-alcoholic fatty liver diseaseNBR1, BRCA1 gene 1 proteinNCoR1, nuclear receptor co-repressor 1NDP52, calcium-binding and coiled-coil domain-containing protein 2NPC-1, Niemann-Pick disease, type C1Nutrient regenerationOPTN, optineurinPEX5, peroxisomal biogenesis factor 5PI3K, phosphatidylinositol-4,5-bisphosphate 3-kinasePINK1, phosphatase and tensin homolog (PTEN)-induced kinase 1PKA, protein kinase APKB, protein kinase BPLIN2, perilipin 2PLIN3, perilipin 3PP2A, protein phosphatase 2aPPARα, peroxisomal proliferator-activated receptor-alphaPQLC2, PQ-loop proteinPXR, pregnane X receptorQuality controlRETREG1, reticulophagy regulator 1ROS, reactive oxygen speciesRTN3, reticulon 3RTNL3, a long isoform of RTN3S1PR2, sphingosine-1-phosphate receptor 2S6K, P70-S6 kinaseS6RP, S6 ribosomal proteinSCARB2, scavenger receptor class B member 2SEC62, SEC62 homolog, preprotein translocation factorSignaling proteinsSIRT1, sirtuin 1SLC36A1, solute carrier family 36 member 1SLC38A7, solute carrier family 38 member 7SLC38A9, sodium-coupled neutral amino acid transporter 9SNAT7, sodium-coupled neutral amino acid transporter 7SPIN, spindlingSQSTM1, sequestosome 1STBD1, starch-binding domain-containing protein 1TBK1, serine/threonine-protein kinaseTEX264, testis expressed 264, ER-phagy receptorTFEB/TFE3, transcription factor EBTGR5, takeda G protein receptor 5TRAC-1, thyroid-hormone-and retinoic acid-receptor associated co-repressor 1TRPML1, transient receptor potential mucolipin 1ULK1, Unc-51 like autophagy activating kinase 1UPR, unfolded protein responseV-ATPase, vacuolar-ATPaseVDR, vitamin D3 receptorVLDL, very-low-density lipoproteinWIPI1, WD repeat domain phosphoinositide-interacting protein 1

Identifiers

PMID35127371
PMCPMC8799888
OpenAlexW3183146269

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.