Evidence map›Paper›PMID 38156441›Full record

ReviewExpert opinion on therapeutic targets

Powering down the mitochondrial LonP1 protease: a novel strategy for anticancer therapeutics.

Rahul Shetty, Roberto Noland, Ghata Nandi, Carolyn K Suzuki

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Exercise attenuates polycystic ovary syndrome development via improved mitochondrial proteostasis.American journal of physiology. Endocrinology and metabolism · 2026
    Article
  6. Article
  7. Metabolic reprogramming as a key regulator in Helicobacter pylori-infected gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. The Role of N6-Methyladenosine in Mitochondrial Dysfunction and Pathology.International journal of molecular sciences · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
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

4 authors at 2 institutions in 1 country.

Rahul ShettyDepartment of Microbiology, Biochemistry & Molecular Genetics, Rutgers University- New Jersey Medical School, Newark, NJ, USA.
Roberto NolandDepartment of Microbiology, Biochemistry & Molecular Genetics, Rutgers University- New Jersey Medical School, Newark, NJ, USA.
Ghata NandiDepartment of Microbiology, Biochemistry & Molecular Genetics, Rutgers University- New Jersey Medical School, Newark, NJ, USA.
Carolyn K SuzukiDepartment of Microbiology, Biochemistry & Molecular Genetics, Rutgers University- New Jersey Medical School, Newark, NJ, USA.
Rutgers New Jersey Medical SchoolRutgers, The State University of New Jersey · US

Funding

Mitochondrial metabolism and the Lon-PDH axisR01GM136905 · NIGMS · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI SUZUKI, CAROLYN K · 2020 to 2023
$1.6M
High throughput screens for modulators of mitochondrial ATP-dependent proteolysisR01GM084039 · NIGMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SUZUKI, CAROLYN K · 2009 to 2010
$734k
High throughput screening assays to identify small molecules that target the ClpXR21NS067668 · NINDS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SUZUKI, CAROLYN K · 2010 to 2010
$171k
NIGMS NIH HHS R01 GM084039NIGMS NIH HHS R01 GM136905NINDS NIH HHS R21 NS067668
6 · The paper itself

Abstract

introductionMitochondrial LonP1 is an ATP-powered protease that also functions as an ATP-dependent chaperone. LonP1 plays a pivotal role in regulating mitochondrial proteostasis, metabolism and cell stress responses. Cancer cells exploit the functions of LonP1 to combat oncogenic stressors such as hypoxia, proteotoxicity, and oxidative stress, and to reprogram energy metabolism enabling cancer cell proliferation, chemoresistance, and metastasis. AREAS COVERED: LonP1 has emerged as a potential target for anti-cancer therapeutics. We review how cytoprotective functions of LonP1 can be leveraged by cancer cells to support oncogenic growth, proliferation, and survival. We also offer insights into small molecule inhibitors that target LonP1 by two distinct mechanisms: competitive inhibition of its protease activity and allosteric inhibition of its ATPase activity, both of which are crucial for its protease and chaperone functions. EXPERT OPINION: We highlight advantages of identifying specific, high-affinity allosteric inhibitors blocking the ATPase activity of LonP1. The future discovery of such inhibitors has potential application either alone or in conjunction with other anticancer agents, presenting an innovative approach and target for cancer therapeutics.

Indexed as

Energy MetabolismPeptide HydrolasesAdenosine TriphosphatasesAdenosine TriphosphateCell ProliferationHumansAdenosine TriphosphatasesAdenosine TriphosphatePeptide HydrolasesAAA+ proteaseallosteric inhibitorATP-powered proteaseCancerCDDO-MeLonP1Lon proteasemitochondria

Identifiers

PMID38156441
PMCPMC10939840
OpenAlexW4390405895

What OpenQuestion holds

Textmetadata
LicenceTDM
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.