Evidence map›Paper›PMID 36860271›Full record

ReviewAnimal cells and systems2023

Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases.

Junhee Kwon, Jihyun Kim, Keun Il Kim

Open access · goldAbstract readReview
In one paragraph

Review in Animal cells and systems, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
12.9field-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

52 citing papers in PubMed, 60 citations in OpenAlex.

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  17. Oxidative Stress in Heat Stress Nephropathy: Crosstalk.Oxidative medicine and cellular longevity · 2026
    Review
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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

3 authors at 1 institution in 1 country.

Junhee KwonDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.ORCID https://orcid.org/0000-0002-6625-1764
Jihyun KimDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.ORCID https://orcid.org/0000-0002-5542-6450
Keun Il KimDepartment of Biological Sciences, Sookmyung Women's University, Seoul, Republic of Korea.ORCID https://orcid.org/0000-0002-9680-6230
Sookmyung Women's University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells activate protective mechanisms to overcome stressful conditions that threaten cellular homeostasis, including imbalances in calcium, redox, and nutrient levels. Endoplasmic reticulum (ER) stress activates an intracellular signaling pathway, known as the unfolded protein response (UPR), to mitigate such circumstances and protect cells. Although ER stress is sometimes a negative regulator of autophagy, UPR induced by ER stress typically activates autophagy, a self-degradative pathway that further supports its cytoprotective role. Sustained activation of ER stress and autophagy is known to trigger cell death and is considered a therapeutic target for certain diseases. However, ER stress-induced autophagy can also lead to treatment resistance in cancer and exacerbation of certain diseases. Since the ER stress response and autophagy affect each other, and the degree of their activation is closely related to various diseases, understanding their relationship is very important. In this review, we summarize the current understanding of two fundamental cellular stress responses, the ER stress response and autophagy, and their crosstalk under pathological conditions to help develop therapies for inflammatory diseases, neurodegenerative disorders, and cancer.

Indexed as

autophagyEndoplasmic reticulum (ER) stresshuman diseasesunfolded protein response (UPR)

Identifiers

PMID36860271
PMCPMC9970256
OpenAlexW4321612721

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.