Evidence map›Paper›PMID 27430889›Full record

ReviewScience China. Life sciences2016

Regulation of lysosomal ion homeostasis by channels and transporters.

Jian Xiong, Michael X Zhu

Open access · hybridAbstract readReview
In one paragraph

Review in Science China. Life sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
11.3field-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

76 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. ATP13A2 restrains macrophage NLRP3 inflammasome activation to repress neurodegeneration via modulating mitochondrial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
  11. Possible Roles for Purinergic Receptor P2RX4 in Breast and Prostate Cancers.International journal of molecular sciences · 2025
    Review
  12. CaBiomolecules · 2025
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

16 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

2 authors at 1 institution in 1 country.

Jian XiongDepartment of Integrative Biology and Pharmacology, McGovern Medical School, Program of Cell and Regulatory Biology, Graduate School of Biomedical Sciences, The University of Texas Health Science Center at Houston, Houston, 77030, USA.
Michael X ZhuDepartment of Integrative Biology and Pharmacology, McGovern Medical School, Program of Cell and Regulatory Biology, Graduate School of Biomedical Sciences, The University of Texas Health Science Center at Houston, Houston, 77030, USA. Michael.x.zhu@uth.tmc.edu.
The University of Texas Health Science Center at Houston · US

Funding

Excitatory neurotransmission by PTX-sensitive G proteinsR01NS092377 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ZHU, MICHAEL X · 2015 to 2019
$1.7M
NINDS NIH HHS R01 NS092377
6 · The paper itself

Abstract

Lysosomes are the major organelles that carry out degradation functions. They integrate and digest materials compartmentalized by endocytosis, phagocytosis or autophagy. In addition to more than 60 hydrolases residing in the lysosomes, there are also ion channels and transporters that mediate the flux or transport of H(+), Ca(2+), Na(+), K(+), and Cl(-) across the lysosomal membranes. Defects in ionic exchange can lead to abnormal lysosome morphology, defective vesicle trafficking, impaired autophagy, and diseases such as neurodegeneration and lysosomal storage disorders. The latter are characterized by incomplete lysosomal digestion and accumulation of toxic materials inside enlarged intracellular vacuoles. In addition to degradation, recent studies have revealed the roles of lysosomes in metabolic pathways through kinases such as mechanistic target of rapamycin (mTOR) and transcriptional regulation through calcium signaling molecules such as transcription factor EB (TFEB) and calcineurin. Owing to the development of new approaches including genetically encoded fluorescence probes and whole endolysosomal patch clamp recording techniques, studies on lysosomal ion channels have made remarkable progress in recent years. In this review, we will focus on the current knowledge of lysosome-resident ion channels and transporters, discuss their roles in maintaining lysosomal function, and evaluate how their dysfunction can result in disease.

Indexed as

HomeostasisHumansHydrogen-Ion ConcentrationIntracellular MembranesIon ChannelsIonsIon TransportLysosomesMembrane Transport ProteinsModels, BiologicalIon ChannelsIonsMembrane Transport Proteinscalciumion homeostasislysosomal storage disease (LSD)lysosome acidification

Identifiers

PMID27430889
PMCPMC5147046
OpenAlexW2495355796

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.