Evidence map›Paper›PMID 33671306›Full record

ReviewCells2021

Potential Treatment of Lysosomal Storage Disease through Modulation of the Mitochondrial-Lysosomal Axis.

Myeong Uk Kuk, Yun Haeng Lee, Jae Won Kim, Su Young Hwang, Joon Tae Park, Sang Chul Park

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  3. Cystinosis and Cellular Energy Failure: Mitochondria at the Crossroads.International journal of molecular sciences · 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

6 authors at 2 institutions in 1 country.

Myeong Uk KukDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Korea.
Yun Haeng LeeDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Korea.
Jae Won KimDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Korea.
Su Young HwangDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Korea.
Joon Tae ParkDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Korea.ORCID 0000-0003-2396-9108
Sang Chul ParkThe Future Life & Society Research Center, Chonnam National University, Gwangju 61186, Korea.
Incheon National University · KRChonnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysosomal storage disease (LSD) is an inherited metabolic disorder caused by enzyme deficiency in lysosomes. Some treatments for LSD can slow progression, but there are no effective treatments to restore the pathological phenotype to normal levels. Lysosomes and mitochondria interact with each other, and this crosstalk plays a role in the maintenance of cellular homeostasis. Deficiency of lysosome enzymes in LSD impairs the turnover of mitochondrial defects, leading to deterioration of the mitochondrial respiratory chain (MRC). Cells with MRC impairment are associated with reduced lysosomal calcium homeostasis, resulting in impaired autophagic and endolysosomal function. This malicious feedback loop between lysosomes and mitochondria exacerbates LSD. In this review, we assess the interactions between mitochondria and lysosomes and propose the mitochondrial-lysosomal axis as a research target to treat LSD. The importance of the mitochondrial-lysosomal axis has been systematically characterized in several studies, suggesting that proper regulation of this axis represents an important investigative guide for the development of therapeutics for LSD. Therefore, studying the mitochondrial-lysosomal axis will not only add knowledge of the essential physiological processes of LSD, but also provide new strategies for treatment of LSD.

Indexed as

AutophagyDisease ProgressionHomeostasisHumansLysosomal Storage DiseasesLysosomesMitochondrialysosomal storage diseaselysosomemitochondriamitochondrial–lysosomal axis

Identifiers

PMID33671306
PMCPMC7921977
OpenAlexW3132836667

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.