Evidence map›Paper›PMID 40520648›Full record

ReviewAPL bioengineering2025

Decoding force-transmission linkages for therapeutic targeting and engineering.

Jingzhun Liu, Yunxin Deng, Jie Yan

Abstract readReview
In one paragraph

Review in APL bioengineering, 2025. 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. 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

3 authors.

Jingzhun LiuDepartment of Physics, National University of Singapore, Singapore 117542, Singapore.ORCID https://orcid.org/0000-0003-4585-8310
Yunxin DengMechanobiology Institute, National University of Singapore, Singapore 117411, Singapore.ORCID https://orcid.org/0009-0004-0267-4153

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanosensing and mechanotransduction enable cells to perceive and respond to mechanical forces, underpinning essential physiological processes and disease pathways. Central to these phenomena are force-transmission supramolecular linkages, which undergo structural transitions and regulate signaling proteins in response to mechanical stimuli. This review examines the mechanisms of these force-bearing linkages, focusing on force duration, dictated by the stability of protein-protein interfaces, and force-dependent mechanical structural changes of force-bearing domains in the linkage, which activates or deactivates mechanosensing domains. We discuss the emerging potential of these linkages as pharmaceutical targets, exploring drugs and peptides designed to modulate these mechanical properties. In addition, we highlight the application of artificial intelligence in protein engineering to enhance therapeutic precision by dynamically tuning these mechanosensing characteristics. Our synthesis of current findings and future perspectives aims to inform novel approaches to drug design and inspire future research in the field of mechanomedicine.

Identifiers

PMID40520648
PMCPMC12166987

What OpenQuestion holds

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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.