Evidence map›Paper›PMID 42855640›Full record

ReviewEuropean journal of pediatrics2026

Hepatic manifestations of ciliopathies: genetic causes and clinical update.

Robert Hegarty, Yoh Zen, John A Sayer

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In one paragraph

Review in European journal of pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Robert HegartyPaediatric Liver, GI and Nutrition Centre, King's College Hospital NHS Foundation Trust, London, SE5 9RS, UK. roberthegarty@nhs.net.ORCID https://orcid.org/0000-0002-5893-6464
Yoh ZenInstitute of Liver Studies, King's College Hospital, London, UK.
John A SayerBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Central Parkway, Newcastle Upon Tyne, NE1 3BZ, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ciliopathies are genetically heterogeneous disorders of primary cilia that frequently involve the liver in childhood, producing a spectrum of hepatobiliary pathology. Primary cilia on cholangiocytes and hepatic progenitors are mechano-, chemo-, and osmo-sensors essential for remodelling of the ductal plate, the embryologic precursor of the liver's intrahepatic bile duct system. Disruption of the components of primary cilia (basal body, intraflagellar transport (IFT), transition-zone, trafficking, and endoplasmic reticulum (ER)/Golgi protein homeostasis components) leads to ductal plate malformation, aberrant biliary branching, and progressive periductal fibrosis. Classical loci (PKHD1, PKD1, PKD2) more commonly associated with cystic kidney disease remain central to aetiology, while ER/glycosylation protein homeostasis genes (GANAB, ALG8, PRKCSH, SEC63, DNAJB11), trafficking/IFT-A and WDR/dynein-2 components (TULP3, WDR family) are increasingly recognised. Liver disease most often appears from childhood to adolescence in autosomal recessive polycystic kidney disease (ARPKD), Bardet-Biedl syndrome, Joubert syndrome, and WDR-related disorders, while autosomal dominant polycystic kidney and liver disease (ADPKD and ADPLD) usually presents in adulthood. The main disease patterns also vary: congenital hepatic fibrosis and portal hypertension in ARPKD, hepatic cysts in ADPKD, steatotic liver disease in Bardet-Biedl syndrome, and transaminitis or fibrocystic liver disease in Joubert and WDR-related disorders. Emerging contributors such as DCDC2 and PKD1L1 implicate microtubule-cilium interactions and mechanosensory dysfunction in neonatal cholestasis and biliary atresia. Diagnosis increasingly relies on broad multigene panels or exome/genome sequencing, with functional assays guiding interpretation of novel alleles.

conclusionThis narrative review synthesises contemporary knowledge on ciliary roles in biliary development, the clinical hepatic phenotypes observed in children and adults, and the evolving genetic landscape with emphasis on discoveries from recent sequencing cohorts and functional studies. WHAT IS KNOWN: • Ciliopathies are genetically heterogeneous disorders in which primary cilia dysfunction disrupts cholangiocyte signalling and ductal plate remodelling, leading to a spectrum of paediatric hepatobiliary disease ranging from congenital hepatic fibrosis and portal hypertension to cystic liver disease, steatotic liver disease, and neonatal cholestasis. WHAT IS NEW: • Recent genomic and functional studies have broadened the spectrum of ciliopathy-associated genes implicated in paediatric hepatic disease. Clinicians caring for these children should maintain a high index of suspicion as the range of reported phenotypes continues to expand.

Indexed as

CiliopathiesLiver DiseasesChildCiliaHumansCiliopathyCongenital hepatic fibrosisDuctal plate malformationGenetic testingLiverMolecular geneticsPaediatricsPolycystic liver disease

Identifiers

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Registered trials

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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.