Evidence map›Paper›PMID 41961943›Full record

ArticleScience advances2026

Targeting mitocytosis potentiates mitochondria drug delivery for antimetastasis therapy.

Yudi Deng, Yunhui Zhang, Fuya Jia, Peihang Jiang, Lian Li, Yuan Huang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Yudi DengKey Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu 610041, China.ORCID 0000-0002-9080-1674
Yunhui ZhangKey Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu 610041, China.
Fuya JiaKey Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu 610041, China.
Peihang JiangKey Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu 610041, China.ORCID 0009-0005-2383-1020
Lian LiKey Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu 610041, China.ORCID 0000-0002-3616-8206
Yuan HuangKey Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu 610041, China.ORCID 0000-0003-3410-8602

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitocytosis is a compensatory pathway responding to mitochondria stress in migratory cells, which expels damaged mitochondria through migrasomes, preserving mitochondrial homeostasis and cellular viability. We found distinct responses to mitochondria-targeted therapy across breast tumor models distinguished by migrasome expression (4T1 > E0771 > EMT6). The antimetastatic efficacy of mitochondrial damage was notably compromised in the migrasome-high 4T1 tumor model due to robust mitocytosis activation, which is merely explored and lacks effective strategy. Here, we developed a mitochondria-targeted nanoplatform (RH-NPs) with the functions of mitocytosis inhibition and mitochondrial damage. Mitochondria-targeted triphenylphosphonium-modified lonidamine (TPP-LND) and integrin inhibitor cilengitide (CGT) were separately loaded into a nanodelivery system (TL/RH-NPs and CGT/RH-NPs, respectively). TL/RH-NPs effectively targeted and damaged tumor mitochondria. Simultaneously, upon mitocytosis activation, CGT/RH-NPs hitchhiked with damaged mitochondria into migrasomes to block mitocytosis via integrin inhibition. This strategy significantly potentiated antimetastatic efficacy in 4T1 tumor models, which established an effective approach for mitocytosis modulation and optimization of mitochondria-targeted therapies.

Indexed as

Antineoplastic AgentsBreast NeoplasmsDrug Delivery SystemsMitochondriaAnimalsCell Line, TumorCell MovementFemaleHumansIndazolesMiceNanoparticlesNeoplasm MetastasisAntineoplastic AgentsIndazoleslonidamine

Identifiers

PMID41961943
PMCPMC13068050

What Socratic 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 Socratic graph.