ArticleJournal of translational internal medicine2026
Immunoglobulin κ drives liver regeneration by stabilizing MYLK to maintain cytoskeletal integrity and promote hepatocyte proliferation.
Article in Journal of translational internal medicine, 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
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.
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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Objectives: Liver regeneration necessitates coordinated cytoskeletal dynamics, yet the key molecular orchestrators remain incompletely defined. Intriguingly, recent studies reveal a novel role for hepatocyte-derived Igκ in promoting hepatocyte survival during liver injury. However, the precise mechanisms by which immunoglobulin κ (Igκ) governs liver regeneration and its potential as a central coordinator remain elusive. This study aims to elucidate the role of Igκ in liver regeneration following injury and to define the underlying molecular mechanisms. Methods: Igκ expression was assessed in liver biopsies from patients with drug-induced liver injury (DILI) using immunohistochemistry. To investigate its role in regeneration, hepatocyte-specific Igκ-knockout mice were subjected to partial hepatectomy (PHx) or acetaminophen (APAP)-induced acute liver injury. Functional and mechanistic studies were performed in the normal human hepatocyte cell line THLE-2 through Igκ knockdown or overexpression, combined with multi-omics profiling, immunoprecipitation, and mass spectrometry. The therapeutic potential of Igκ was validated by AAV8-mediated hepatic delivery of Igκ in knockout mice. Results: Igκ expression is significantly upregulated in both human DILI patients and murine injury models upon hepatic damage. Hepatocyte-specific Igκ deletion impaired liver regeneration, characterized by disrupted cytoskeletal organization and diminished hepatocyte proliferation. Mechanistically, Igκ directly binds to myosin light chain kinase (MYLK), shielding it from K48-linked ubiquitination and proteasomal degradation, thereby preserving cytoskeletal integrity and facilitating Yes-associated protein (YAP) nuclear translocation to activate proliferative pathways. Crucially, AAV8-mediated hepatic Igκ delivery in knockout mice rescues MYLK protein levels, restores cytoskeletal integrity, and promotes liver regeneration. Conclusions: Our study identifies Igκ as a pivotal regulator of liver regeneration by stabilizing MYLK to maintain cytoskeletal dynamics and potentiate YAP-dependent proliferative signaling, thereby proposing a potential therapeutic strategy for enhancing hepatic repair.
Indexed as
Identifiers
What OpenQuestion holds
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.