EPRS1 and Kidney Fibrosis
Author Information
Author(s): Son Seung Seob, Jeong Hee Seul, Lee Seong-Woo, Lee Eun Soo, Lee Jeong Geon, Lee Ji-Hye, Yi Jawoon, Park Mi Ju, Choi Min Sun, Lee Donghyeong, Choi Sin Young, Ha Jiheon, Kang Jeong Suk, Cho Nam-Jun, Park Samel, Gil Hyo-Wook, Chung Choon Hee, Park Joon Seok, Kim Myung Hee, Park Jihwan, Lee Eun Young
Primary Institution: Soonchunhyang University
Hypothesis
EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis.
Conclusion
Targeting EPRS1 could be a potential therapeutic strategy for alleviating kidney fibrosis and dysfunction.
Supporting Evidence
- EPRS1 levels were increased in fibrotic kidneys of patients and mice.
- EPRS1 inhibition protected against kidney fibrosis and dysfunction.
- EPRS1 promotes fibrosis by activating fibroblasts and causing mitochondrial dysfunction.
- Inhibiting EPRS1 reduced collagen production and improved kidney function.
- EPRS1 is linked to both TGF-β and JAK-STAT pathways.
- EPRS1 inhibition improved mitochondrial function in kidney cells.
- Targeting EPRS1 may provide a new treatment for chronic kidney disease.
- Future research may explore EPRS1 inhibitors as potential therapies.
Takeaway
EPRS1 is an enzyme that helps make proteins, and when it works too much, it can cause kidney problems. Scientists found that blocking EPRS1 can help fix these kidney issues.
Methodology
The study involved patients, mice, and in vitro cells, using techniques like immunohistochemistry, western blot, and single-cell RNA sequencing.
Limitations
The study did not assess the toxicity of the EPRS1 inhibitor in the specific mouse model used.
Participant Demographics
Six patients, including three with focal segmental glomerulosclerosis.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website