ArticleeLife2022
Hypoxia-inducible factor underlies von Hippel-Lindau disease stigmata.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Von Hippel-Lindau Syndrome: An Updated Narrative Review for the First-Contact Clinician.Cureus · 2026Review
- Article
- E3 ubiquitin ligases in signaling, disease, and therapeutics.Trends in biochemical sciences · 2025Review
- Article
- Diagnosis and treatment of Von Hippel-Lindau syndrome: A case series.Experimental and therapeutic medicine · 2025Article
- The hypoxic response extends lifespan through a bioaminergic and peptidergic neural circuit.bioRxiv : the preprint server for biology · 2025Article
- Influence of Hypoxia on the Airway Epithelium.Physiological research · 2024Review
- Glucose deprivation impairs hypoxia-inducible factor-1α synthesis.Discover oncology · 2024Article
- Review
- Genetics, Pathophysiology, and Current Challenges in Von Hippel-Lindau Disease Therapeutics.Diagnostics (Basel, Switzerland) · 2024Review
- Saturation genome editing maps the functional spectrum of pathogenic VHL alleles.Nature genetics · 2024Article
- Cathepsins L and B target HIF1α for oxygen-independent proteolytic cleavage.Scientific reports · 2024Article
- Belzutifan-induced regression of retinal capillary hemangioblastoma: A case-series.American journal of ophthalmology case reports · 2024Article
- Deficiency in PHD2-mediated hydroxylation of HIF2α underlies Pacak-Zhuang syndrome.Communications biology · 2024Article
- Tumour response to hypoxia: understanding the hypoxic tumour microenvironment to improve treatment outcome in solid tumours.Frontiers in oncology · 2024Review
- Targeting the SMURF2-HIF1α axis: a new frontier in cancer therapy.Frontiers in oncology · 2024Review
- Structural basis for binding of the renal carcinoma target hypoxia-inducible factor 2α to prolyl hydroxylase domain 2.Proteins · 2023Article
- While paradigms shift in von Hippel-Lindau management, questions remain in optimal multidisciplinary neuro-oncology care.Neuro-oncology · 2023Article
- Structural Characterization of Hypoxia Inducible Factor α-Prolyl Hydroxylase Domain 2 Interaction through MD Simulations.International journal of molecular sciences · 2023Article
- Identification of gene signatures related to hypoxia and angiogenesis in pancreatic cancer to aid immunotherapy and prognosis.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
von Hippel-Lindau (VHL) disease is a rare hereditary cancer syndrome that causes a predisposition to renal clear-cell carcinoma, hemangioblastoma, pheochromocytoma, and autosomal-recessive familial polycythemia. pVHL is the substrate conferring subunit of an E3 ubiquitin ligase complex that binds to the three hypoxia-inducible factor alpha subunits (HIF1-3α) for polyubiquitylation under conditions of normoxia, targeting them for immediate degradation by the proteasome. Certain mutations in pVHL have been determined to be causative of VHL disease through the disruption of HIFα degradation. However, it remains a focus of investigation and debate whether the disruption of HIFα degradation alone is sufficient to explain the complex genotype-phenotype relationship of VHL disease or whether the other lesser or yet characterized substrates and functions of pVHL impact the development of the VHL disease stigmata; the elucidation of which would have a significant ramification to the direction of research efforts and future management and care of VHL patients and for those manifesting sporadic counterparts of VHL disease. Here, we examine the current literature including the other emergent pseudohypoxic diseases and propose that the VHL disease-phenotypic spectrum could be explained solely by the varied disruption of HIFα signaling upon the loss or mutation in pVHL.
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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.