Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Transcriptional activation of PINK1 by MyoD1 mediates mitochondrial homeostasis to induce renal calcification in pediatric nephrolithiasis

6 Sept 2024

Abstract excerpt

This study aims to uncover the molecular mechanisms underlying pediatric kidney stone formation induced by renal calcium deposition by utilizing high-throughput sequencing data to reveal the regulation of PINK1 by MyoD1. We performed transcriptome sequencing on peripheral blood samples from healthy children and children with kidney stones to obtain differentially expressed genes (DEGs). Genes related to...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Ion Transport and Channel Regulation
Share to Kidney Stones and Urolithiasis Treatments
Share to Parathyroid Disorders and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 39242558
DOI: 10.1038/s41420-024-02117-w

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Transcriptional activation of PINK1 by MyoD1 mediates mitochondrial homeostasis to induce renal calcification in pediatric nephrolithiasisPMID 39242558Read ↗

Integrative genome-wide analyses identify novel loci associated with kidney stones and provide insights into its genetic architecture.Semantic proximity Read ↗

Genetic susceptibility to kidney stone disease: unveiling pathogenesis and potential therapeutic targets.Semantic proximity Read ↗

Identification of the pivotal role of SPP1 in kidney stone disease based on multiple bioinformatics analysisSemantic proximity Read ↗

Uncovering the mechanisms of diosmin in treating obesity-related kidney injury based on network pharmacology, molecular docking, and in vitro validationSemantic proximity Read ↗

Genome-Wide Gene Expression Profiling of Randall’s Plaques in Calcium Oxalate Stone FormersSemantic proximity Read ↗

DDIT4 mediated autophagy and ferroptosis through VDR-mTOR signaling pathway in the treatment of diabetic kidney diseaseSemantic proximity Read ↗

Loss of Fnip1 alters kidney developmental transcriptional program and synergizes with TSC1 loss to promote mTORC1 activation and renal cyst formation.Semantic proximity Read ↗

Meta-analysis of polycystic kidney disease expression profiles defines strong involvement of injury repair processes.Semantic proximity Read ↗

Causal Relationship Between Serum Zinc Levels and Diabetic Kidney Disease (DKD): A Plasma Proteomics Mediation Study.Semantic proximity Read ↗

Regulation of Mitochondrial Oxidative Metabolism by Tumor Suppressor FLCNSemantic proximity Read ↗

PGC-1α in Disease: Recent Renal Insights into a Versatile Metabolic RegulatorSemantic proximity Read ↗

Systems biology approach to identify transcriptome reprogramming and candidate microRNA targets during the progression of polycystic kidney disease.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.