How nutrient signals at ER–mitochondria junctions affect mitochondrial health with age
Nutrient signaling at ER-Mitochondrial contacts and age-related mitochondrial dysfunction
['FUNDING_R01'] · UNIVERSITY OF CALIFORNIA LOS ANGELES · NIH-11327390
This work explores whether nutrient signals at spots where mitochondria and the endoplasmic reticulum meet help mitochondria keep working better as people age.
Quick facts
| Phase | ['FUNDING_R01'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | UNIVERSITY OF CALIFORNIA LOS ANGELES (nih funded) |
| Locations | 1 site (LOS ANGELES, UNITED STATES) |
| Trial ID | NIH-11327390 on ClinicalTrials.gov |
What this research studies
Researchers will examine how fasting and nutrient signals change mitochondrial shape and energy use by focusing on protein complexes at endoplasmic reticulum–mitochondria contact sites (MAMs). The team will study how the nutrient-responsive complex mTORC2 and its regulator Rictor influence mitochondrial fission and respiration, and whether mTORC2 activity declines with age. Experiments will use cell cultures and intact mammalian systems, including genetically modified mouse liver models, to measure mitochondrial dynamics and function. The goal is to explain why broad mTOR inhibitors like rapamycin can have mixed effects and to identify more targeted approaches to protect mitochondria during aging.
Who could benefit from this research
Good fit: Older adults or people with age-related mitochondrial problems or related conditions could be candidates for future human studies informed by this work.
Not a fit: People whose conditions do not involve age-related mitochondrial dysfunction or ER–mitochondria signaling are unlikely to receive direct benefit from this basic-science project.
Why it matters
Potential benefit: If successful, this work could point to ways to preserve mitochondrial function in aging tissues and guide safer treatments that target nutrient-signaling pathways.
How similar studies have performed: Previous cell and animal studies have shown fasting and pathways like AMPK affect mitochondrial dynamics, but the role of mTORC2 in fasting-driven fission and age-related decline is relatively new and not yet established in humans.
Where this research is happening
LOS ANGELES, UNITED STATES
- UNIVERSITY OF CALIFORNIA LOS ANGELES — LOS ANGELES, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: SINGH, RAJAT — UNIVERSITY OF CALIFORNIA LOS ANGELES
- Study coordinator: SINGH, RAJAT
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.