Leptin mitigates heat stress-induced senescence in porcine Sertoli cells through modulation of ATM-p53, ERK1/2, and AMPK-mTORC1 signaling

Clicks: 12
ID: 330029
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #452 of 847 articles by views in italian journal of animal science

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 847 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Mammalian spermatogenesis is highly sensitive to temperature fluctuations. Sertoli cells provide essential support for germ cell development and are vulnerable to heat stress-induced cellular damage. Heat stress, known to impair spermatogenesis and induce cellular senescence in various cells, poses a significant threat to male fertility. Given that leptin possesses anti-senescence potential, this study investigates its ability to alleviate heat stress-induced senescence in Sertoli cells and explores the underlying molecular mechanisms. Our results demonstrate that heat stress triggers accumulation of reactive oxygen species (ROS) (P < 0.05), resulting in DNA damage that ultimately drives Sertoli cell senescence. Leptin effectively mitigates senescence through multiple pathways. Specifically, leptin enhances antioxidant enzyme activity (P < 0.05) and inhibits the ATM-p53 pathway, thereby reducing DNA damage. Furthermore, leptin activates the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, reversing G1 phase arrest. Additionally, leptin promotes autophagy via the AMPK-mTORC1 pathway. Concurrently, leptin reduces the activity of senescence-associated β-galactosidase (SA-β-gal) and lessens the release of senescence-associated secretory phenotype (SASP) factors (P < 0.05), thus slowing senescence progression. In conclusion, leptin exerts a protective effect against heat stress-induced senescence in Sertoli cells, offering novel insights into potential strategies for the prevention of heat stress-related male infertility.
Reference Key
openalex_W7214575350 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Ming Guo, Yawen Gao, Jinyang Zhang, Zhendong Zhu, Yan Lin, Lu HongZhao, Jia Cheng, Tao Zhang, Jun Luo, Wenxian Zeng
Are you one of these authors? Claim your profile
Journal italian journal of animal science
Year 2026
DOI
10.1093/jas/skag314
URL
https://doi.org/10.1093/jas/skag314
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.