ReviewCells2024
Alkaptonuria: From Molecular Insights to a Dedicated Digital Platform.
Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed.
- Plasma Proteomic Signatures in Alkaptonuria.Biology · 2026Article
- HGA-Induced Oxidative Stress Impairs Autophagy via Lysosomal Dysfunction in Alkaptonuria.Antioxidants (Basel, Switzerland) · 2026Article
- Ochronotic Deposition in Alkaptonuria: Semiquinone-Mediated Oxidative Coupling and Metabolic Drivers of Homogentisic Acid Accumulation.International journal of molecular sciences · 2025Article
- Treatment of Ochronotic Osteoarthropathy and the Evaluation of Selected Lower Limb Muscle Properties, Including the Patellar Tendon: A Case Report and Mini Literature Review.Journal of clinical medicine · 2025Article
- A Comprehensive In Vitro and In Silico Approach for Targeting 4-Hydroxyphenyl Pyruvate Dioxygenase: Towards New Therapeutics for Alkaptonuria.International journal of molecular sciences · 2025Article
- Ochronotic arthropathy: skeletal manifestations and orthopaedic treatment.EFORT open reviews · 2025Review
- HGA Triggers SAA Aggregation and Accelerates Fibril Formation in the C20/A4 Alkaptonuria Cell Model.Cells · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Alkaptonuria (AKU) is a genetic disorder that affects connective tissues of several body compartments causing cartilage degeneration, tendon calcification, heart problems, and an invalidating, early-onset form of osteoarthritis. The molecular mechanisms underlying AKU involve homogentisic acid (HGA) accumulation in cells and tissues. HGA is highly reactive, able to modify several macromolecules, and activates different pathways, mostly involved in the onset and propagation of oxidative stress and inflammation, with consequences spreading from the microscopic to the macroscopic level leading to irreversible damage. Gaining a deeper understanding of AKU molecular mechanisms may provide novel possible therapeutical approaches to counteract disease progression. In this review, we first describe inflammation and oxidative stress in AKU and discuss similarities with other more common disorders. Then, we focus on HGA reactivity and AKU molecular mechanisms. We finally describe a multi-purpose digital platform, named ApreciseKUre, created to facilitate data collection, integration, and analysis of AKU-related data.
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.