TFAM and mtDNA analysis in AKI patients

Clinical Score: 0.800 Price: $0.50 acute kidney injury human patients Status: proposed

What This Experiment Tests

Clinical experiment designed to assess clinical efficacy targeting TFAM in human patients. Primary outcome: TFAM levels and mtDNA nucleoids in kidney tissue

Description

Clinical study examining kidney tissue samples from acute kidney injury (AKI) patients to validate findings from animal and cell culture models. The study measured TFAM protein levels and mtDNA nucleoid structures in human kidney samples to determine whether the mitochondrial DNA maintenance defects observed in experimental models are also present in human AKI. This translational component aimed to establish clinical relevance of the mechanistic findings and support TFAM as a potential therapeutic target.

TARGET GENE
MODEL SYSTEM
human patients
ESTIMATED COST
$0
TIMELINE
0 months
PATHWAY
mitochondrial DNA maintenance
SOURCE
extracted_from_pmid_33408785
PRIMARY OUTCOME
TFAM levels and mtDNA nucleoids in kidney tissue

Scoring Dimensions

Info Gain 0.00 (25%) Feasibility 0.00 (20%) Hyp Coverage 0.00 (20%) Cost Effect. 0.00 (15%) Novelty 0.00 (10%) Ethical Safety 0.00 (10%) 0.800 composite

📖 Wiki Pages

DNA Damage-Accumulating Neurons in NeurodegeneraticellDNA Methylation Biomarkers in NeurodegenerationbiomarkerDNA Damage Response in Corticobasal SyndromemechanismDNA MethylationentityDNA Damage and Repair in NeuronscellDNA Damage Repair Deficiency Validation Study in PexperimentTFAM GenegeneDNA Damage Repair Deficiency Hypothesis in ParkinshypothesisDNA Damage Repair Therapy - Biomarker GuidedideaDNA Damage Repair Investment LandscapeinvestmentDNA Damage Response in Alzheimer's Diseasemechanismdna-damage-repairmechanismDNA Damage Repair Mechanisms Across NeurodegeneratmechanismDNA Damage Response Impairment PathwaymechanismDNA Damage Response in 4R-Tauopathiesmechanism

Protocol

Analysis of kidney biopsy or tissue samples from AKI patients using immunohistochemistry and/or molecular techniques to assess TFAM expression and mtDNA nucleoid structure

Expected Outcomes

AKI patients would show reduced TFAM levels and damaged mtDNA nucleoids similar to experimental models

Success Criteria

Demonstrable loss of TFAM and mtDNA damage in human AKI kidney samples

Related Hypotheses (2)

TFAM overexpression creates mitochondrial donor-recipient gradients for directed organelle trafficki0.725
Hippocampal mitochondrial dysfunction accelerates with age and drives regional AD vulnerability0.374

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