ReviewMedComm2026
Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.
Review in MedComm, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Hippo pathway and its downstream effectors Yes-associated protein/transcriptional coactivator with PDZ-binding motif-TEA domain transcription factor (YAP/TAZ-TEAD) play critical roles in organ-size control, tissue homeostasis, regeneration, and stem-cell biology. Their aberrant activation drives malignancies, fibrosis, cardiovascular disease, and immune dysregulation. Once regarded undruggable, the YAP/TAZ-TEAD complex has become one of the most actively pursued target classes in oncology and beyond. In this review, we delineate the biological functions of the Hippo-YAP/TAZ-TEAD axis and integrate its pathway physiology with the structural basis of druggability, centered on the Ω-loop surface pocket and the buried palmitoylation-binding pocket (PBP) of TEAD, whose distinct geometries dictate the pharmacophoric requirements, paralog selectivity, and resistance liabilities of current agents. We then systematically compare mechanism-guided therapeutic modalities, encompassing direct protein-protein interaction disruptors, covalent and noncovalent PBP inhibitors, proteolysis-targeting chimeras (PROTACs), and cofactor-interface modulators. We also analyze the upstream kinase (MST1/2, LATS1/2) modulators, direct YAP/TAZ inhibitors and degraders, and emerging gene-, RNA-, antibody-, and cell-based therapies. We critically evaluate preclinical and early clinical performance across oncology, fibrosis, immunology, and regenerative medicine, distinguishing robust proof-of-concept from clinically meaningful benefit. We further dissect resistance mechanisms, on-target safety concerns, and the therapeutic-window limitations of pan-TEAD inhibition. Ultimately, we outline rational combination strategies, biomarker-guided patient selection, and future directions for paralog-selective and tissue-restricted Hippo-targeted therapeutics.
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Registered trials
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.