Evidence map›Paper›PMID 35913019›Full record

ArticleEMBO reports2022

Lysosomal K

Lili Qu, Bingqian Lin, Wenping Zeng, Chunhong Fan, Haotian Wu, Yushu Ge, Qianqian Li, Canjun Li, Yanan Wei, Jing Xin and 3 more

Abstract read
In one paragraph

Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Targeting TMEM175 in Lysosomal Physiology and Human Diseases.Current stem cell research & therapy · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. What We Know About TMEM175 in Parkinson's Disease.CNS neuroscience & therapeutics · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. The ion channels of endomembranes.Physiological reviews · 2024
    Review
  20. 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

13 authors.

Lili Qu *Institute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0001-7811-4508
Bingqian Lin *Institute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-1850-1319
Wenping ZengInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0003-4501-939X
Chunhong FanInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-4554-5261
Haotian WuInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0001-7507-7887
Yushu GeInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-2263-7972
Qianqian LiInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-7903-737X
Canjun LiInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0003-3406-1891
Yanan WeiInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-8294-5715
Jing XinInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-2623-2374
Xingbing WangDepartment of Hematology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-5591-2168
Dan LiuInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0003-4017-3136
Chunlei CangInstitute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-3302-0927

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysosomes are degradative organelles and play vital roles in a variety of cellular processes. Ion channels on the lysosomal membrane are key regulators of lysosomal function. TMEM175 has been identified as a lysosomal potassium channel, but its modulation and physiological functions remain unclear. Here, we show that the apoptotic regulator Bcl-2 binds to and inhibits TMEM175 activity. Accordingly, Bcl-2 inhibitors activate the channel in a caspase-independent way. Increased TMEM175 function inhibits mitophagy, disrupts mitochondrial homeostasis, and increases production of reactive oxygen species (ROS). ROS further activates TMEM175 and thus forms a positive feedback loop to augment apoptosis. In a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease (PD), knockout (KO) of TMEM175 mitigated motor impairment and dopaminergic (DA) neuron loss, suggesting that TMEM175-mediated apoptosis plays an important role in Parkinson's disease (PD). Overall, our study reveals that TMEM175 is an important regulatory site in the apoptotic signaling pathway and a potential therapeutic target for Parkinson's disease (PD).

Indexed as

Parkinson DiseaseAnimalsApoptosisDisease Models, AnimalLysosomesMiceMice, Inbred C57BLPotassium ChannelsProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesPotassium ChannelsProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesTMEM175 protein, mouseapoptosislysosomeParkinson's diseasepotassium channelTMEM175

Identifiers

PMID35913019
PMCPMC9442313

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Registered trials

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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.