Evidence mapPaperPMID 42236674Full record

ReviewSignal transduction and targeted therapy2026

Transcriptional and epigenetic regulation of autophagy: mechanisms, disease relevance and therapeutic opportunities.

Jieun Seo, Seo-Young Park, Dong Chul Lee, Wonbeak Yoo, Yong Ryoul Yang, Hwi Won Seo, Jong Lyul Park, Jae-Yeol Joo, Kyung Chan Park, Sangwon Byun

Abstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

1 citing paper in PubMed.

  1. Review
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

10 authors.

Jieun Seo *Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.
Seo-Young Park *Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.
Dong Chul LeeGenomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.
Wonbeak YooGenomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.
Yong Ryoul YangAging Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.ORCID http://orcid.org/0009-0001-9096-7420
Hwi Won SeoInfectious Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0002-0486-3351
Jong Lyul ParkAging Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.
Jae-Yeol JooDepartment of Pharmacy, College of Pharmacy, Hanyang University, Ansan, Gyeonggi-do, Republic of Korea.
Kyung Chan ParkGenomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea. kpark@kribb.re.kr.
Sangwon ByunGenomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea. swbyun00@kribb.re.kr.

Funding

Korea Research Institute of Bioscience and Biotechnology (KRIBB) KGM5192423Korea Research Institute of Bioscience and Biotechnology (KRIBB) KGM9942522National Research Foundation of Korea (NRF) NRF-2021R1A2C1005368National Research Foundation of Korea (NRF) RS-2023-00217123
6 · The paper itself

Abstract

Autophagy is a tightly regulated catabolic process that is essential for cellular homeostasis, stress adaptation, and metabolic balance. Its dysregulation has been implicated in a wide range of diseases, including cancer, neurodegenerative disorders, metabolic syndromes, muscular diseases, and infections. Recent studies have revealed the central roles of transcription factors, including TFEB, FOXO family members, p53, and NF-κB, in orchestrating autophagy through their direct regulation of lysosome-related genes. These factors often interact with epigenetic regulators such as histone acetyltransferases, deacetylases, and methyltransferases, which fine-tune chromatin accessibility and transcriptional output. Dysregulation of these pathways leads to aberrant autophagy and contributes to pathogenesis. Emerging therapeutic strategies targeting these transcriptional and epigenetic regulators have shown promise in preclinical and clinical settings, although challenges remain owing to the context-specific roles of autophagy in promoting either cell survival or cell death or contributing to protein aggregation and metabolic imbalance, depending on the disease. Clinical trials with autophagy modulators, including mTOR inhibitors, HDAC inhibitors, SIRT1 activators, and TFEB agonists, have yielded variable outcomes, emphasizing the need for precision medicine approaches. Advances in nanomedicine and biomaterials provide innovative delivery platforms that increase the specificity, bioavailability, and tissue targeting ability of autophagy-targeting agents. This review provides a comprehensive and detailed synthesis of how transcriptional and epigenetic regulators control autophagy across physiological and pathological contexts. In addition, we discuss therapeutic efforts, challenges in clinical translation, and future directions, including biomarker discovery, combinatorial treatment strategies, and targeted delivery systems, to enable more effective modulation of autophagy in disease.

Indexed as

AutophagyEpigenesis, GeneticNeoplasmsNeurodegenerative DiseasesTranscription, GeneticAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsHumansBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsTFEB protein, human

Identifiers

PMID42236674
PMCPMC13234203

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.