ArticleNature aging2022
Suppression of intestinal dysfunction in a Drosophila model of Parkinson's disease is neuroprotective.
Article in Nature aging, 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, 21 citations in OpenAlex.
- The complement C3-microglial axis in depression of Parkinson's disease: from mechanism to therapeutic intervention.EBioMedicine · 2026Article
- Loss of TDP-43 Drives Innate Immune Activation Through Relish inInternational journal of molecular sciences · 2026Article
- Longitudinal lineage tracing reveals early clonal attrition during Drosophila midgut aging.PLoS biology · 2026Article
- BNIP3-Dependent Mitophagy Non-Autonomously Regulates Systemic Aging via NF-κB Suppression in Drosophila.Aging cell · 2026Article
- Insights into PINK1/Parkin function and dysfunction from Drosophila models.The Biochemical journal · 2025Review
- Neuroprotective Effect of Cannabidiol Against Rotenone in Hippocampal Neuron Culture.Chemistry, an Asian journal · 2025Article
- In vivo and in silico models of Drosophila for Parkinson's disease.The FEBS journal · 2025Review
- Loss of Drosophila ribosomal protein S6 kinase II causes mitochondrial dysfunction and cell death.Disease models & mechanisms · 2025Article
- Drosophila melanogaster models for investigating inflammatory bowel disease: Methods, pathology, mechanisms, and therapeutic approaches.Biomolecules & biomedicine · 2025Review
- Non-Immune Functions of Innate Immunity Acting on Physiological Processes: Insights fromInternational journal of molecular sciences · 2025Review
- Mass spectrometry-based proteomics for biomarker discovery in theNeuroprotection (Chichester, England) · 2024Review
- Enhancing mitochondrial one-carbon metabolism is neuroprotective in Alzheimer's disease models.Cell death & disease · 2024Article
- Emerging roles of antimicrobial peptides in innate immunity, neuronal function, and neurodegeneration.Trends in neurosciences · 2024Review
- The role of PINK1-Parkin in mitochondrial quality control.Nature cell biology · 2024Review
- Modulating p38 MAPK signaling by proteostasis mechanisms supports tissue integrity during growth and aging.Nature communications · 2023Article
- Loss of STING in parkin mutant flies suppresses muscle defects and mitochondria damage.PLoS genetics · 2023Article
- Upregulation of Tribbles decreases body weight and increases sleep duration.Disease models & mechanisms · 2023Article
- Blocking dPerk in the intestine suppresses neurodegeneration in a Drosophila model of Parkinson's disease.Cell death & disease · 2023Article
- Towards early detection of neurodegenerative diseases: A gut feeling.Frontiers in cell and developmental biology · 2023Review
- Neuron-periphery mitochondrial stress communication in aging and diseases.Life medicine · 2022Review
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7 authors at 1 institution in 1 country.
Funding
Abstract
The innate immune response mounts a defense against foreign invaders and declines with age. An inappropriate induction of this response can cause diseases. Previous studies showed that mitochondria can be repurposed to promote inflammatory signaling. Damaged mitochondria can also trigger inflammation and promote diseases. Mutations in pink1, a gene required for mitochondrial health, cause Parkinson's disease, and Drosophila melanogaster pink1 mutants accumulate damaged mitochondria. Here, we show that defective mitochondria in pink1 mutants activate Relish targets and demonstrate that inflammatory signaling causes age-dependent intestinal dysfunction in pink1-mutant flies. These effects result in the death of intestinal cells, metabolic reprogramming and neurotoxicity. We found that Relish signaling is activated downstream of a pathway stimulated by cytosolic DNA. Suppression of Relish in the intestinal midgut of pink1-mutant flies restores mitochondrial function and is neuroprotective. We thus conclude that gut-brain communication modulates neurotoxicity in a fly model of Parkinson's disease through a mechanism involving mitochondrial dysfunction.
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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.