Evidence map›Paper›PMID 42842400›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2026

Cell jamming transition is regulated by mitochondrial pyruvate transport and endocytosis.

Alexandra Bermudez, Zoe Latham, Johnny Diaz, Weihong Yan, Jerry Chen, Dapeng Bi, Andrew S Goldstein, Jimmy K Hu, Neil Y C Lin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 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. Cell jamming transition is regulated by mitochondrial pyruvate transport and endocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Alexandra Bermudez *Mechanical and Aerospace Engineering Department, University of California, Los Angeles, CA 90095.
Zoe Latham *Bioengineering Department, University of California, Los Angeles, CA 90095.ORCID 0009-0007-4850-184X
Johnny DiazDepartment of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, CA 90095.
Weihong YanDepartment of Chemistry and Biochemistry, University of California, Los Angeles, CA 90095.
Jerry ChenBioengineering Department, University of California, Los Angeles, CA 90095.
Dapeng BiDepartment of Physics, Northeastern University, Boston, MA 02115.ORCID 0000-0003-4850-8666
Andrew S GoldsteinDepartment of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, CA 90095.ORCID 0000-0003-0434-9149
Jimmy K HuDivision of Biosystems and Function, School of Dentistry, University of California, Los Angeles, CA 90095.ORCID 0000-0003-1035-0779
Neil Y C LinMechanical and Aerospace Engineering Department, University of California, Los Angeles, CA 90095.ORCID 0000-0002-8653-1894

Funding

AI-Informed Signaling Factor Design for In Vitro Rejuvenating Mesenchymal Stromal CellsR35GM146735 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Neil Lin · 2022 to 2026
$2.3M
Mechanical regulation of transcription in dental epithelial stem cells through cell packing and tissue forcesR01DE030471 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Jimmy Kuang-Hsien Hu · 2022 to 2026
$1.8M
Alfred P. Sloan Foundation (APSF) N/AHHS | NIH | National Institute of Dental and Craniofacial Research (NIDR) R01DE030471HHS | NIH | National Institute of General Medical Sciences (NIGMS) R35GM146735HHS | NIH | National Institute of General Medical Sciences (NIGMS) R35GM15049NIDCR NIH HHS R01 DE030471NIGMS NIH HHS R35 GM146735NSF | BIO | Division of Biological Infrastructure (DBI) DBI-2325121NSF | ENG | Division of Chemical, Bioengineering, Environmental and Transport Systems (CBET) CBET-2244760NSF | ENG | Division of Civil, Mechanical and Manufacturing Innovation (CMMI) CMMI-2029454NSF | MPS | Division of Materials Research (DMR) DMR-2046683NSF | MPS | Division of Physics (PHY) PHY-2019745
6 · The paper itself

Abstract

Epithelial tissues undergo dynamic transitions between fluid-like collective motion and mechanically jammed states during development, injury repair, and disease progression. However, the cellular programs that drive these transitions and regulate collective behavior remain unclear. Using a controlled crowding model integrated with live-cell imaging and time-resolved multiomics, we demonstrate that epithelial crowding triggers early metabolic changes characterized by increased mitochondrial pyruvate anaplerosis that precedes the jamming transition. Restricting mitochondrial pyruvate import increased collective cell motility and delayed jamming in crowded monolayers. This unjammed state is driven by enhanced cytoskeletal remodeling and requires RhoA-myosin II activity. Mechanistically, we show that elevated cytoskeletal signaling promotes macropinocytic uptake, which serves as a required feedback loop to maintain motility. These findings identify mitochondrial pyruvate utilization as an important regulatory input linking metabolic remodeling to the endocytic control of epithelial fluidity.

Indexed as

EndocytosisEpithelial CellsMitochondriaPyruvic AcidAnimalsBiological TransportCell MovementCytoskeletonDogsMetabolic ReprogrammingMyosin Type IIrhoA GTP-Binding ProteinMyosin Type IIPyruvic AcidrhoA GTP-Binding Proteincollective cell migrationepithelial jamming transitionmechanobiology

Identifiers

PMID42842400
PMCPMC13663687

What OpenQuestion holds

Textmetadata
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.