ArticleAging and disease2019
Novel Role of Lck in Leptin-Induced Inflammation and Implications for Renal Aging.
Article in Aging and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Special Issue "Hormone Signaling in Human Health and Diseases".International journal of molecular sciences · 2026Article
- The Dual Role of Cellular Senescence in Macrophages: Unveiling the Hidden Driver of Age-Related Inflammation in Kidney Disease.International journal of biological sciences · 2025Review
- Exploring the potential mechanisms of Rehmannia glutinosa in treating sepsis based on network pharmacology.BMC infectious diseases · 2024Article
- Exploring biomarkers of premature ovarian insufficiency based on oxford nanopore transcriptional profile and machine learning.Scientific reports · 2023Article
- Article
- Article
- Bioinformatics analysis identifies immune-related gene signatures and subtypes in diabetic nephropathy.Frontiers in endocrinology · 2022Article
- Gene signatures of autopsy lungs from obese patients with COVID-19.Clinical nutrition ESPEN · 2021Article
- Review
- Anatomical Transcriptome Atlas of the Male Mouse Reproductive System During Aging.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is associated with increased fat mass and elevated serum leptin levels (hyperleptinemia), causing proinflammation in the kidneys where it plays a primary role in the removal of endogenous leptin from the circulation. Lymphocyte-specific kinase (Lck) is a positive regulator of inflammatory signaling and a potential treatment target for age-related diseases, but its role in leptin signaling is unknown. Here, we investigated how Lck influences hyperleptinemia-induced inflammation in kidney tissues from 6- and 21-month-old rats. Results indicate that Lck expression and activation increased significantly in aged rat kidneys, especially at renal tubules. Furthermore, we identified interactions between Lck and short leptin-receptor isoforms, suggesting that Lck is a protein tyrosine kinase regulating leptin signaling. We further investigated whether increased Lck expression in renal tubular epithelial cells and macrophage infiltration are associated with leptin-induced inflammation. We then demonstrated that leptin activates Lck and proinflammatory transcription factors (STAT3 and NF-κB), while Lck knockdown modulates the expression of both transcription factors. Collectively, these data implicate that Lck leads to development of leptin-induced renal inflammation during aging. Inhibition of this protein tyrosine kinase may therefore be an appropriate therapeutic option for protection against age-related hyperleptinemia.
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