ArticlePloS one2025
Curcumin ameliorates aging-induced blood-testis barrier disruption by regulating AMPK/mTOR mediated autophagy.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Targeting programmed cell death in male infertility: pathogenic mechanisms and therapeutic strategies.Molecular biology reports · 2026Review
- Neuronal death and accumulation of lipid droplets and glycogen granules within retinal pigment epithelium under the influence of mTOR and autophagy.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Targeting AMPK Networks for Male Reproductive Health: Mechanisms and Emerging Therapies.Cells · 2026Review
- Inflammaging: Immune-Metabolic Crosstalk Between the Prostate-Testis and Musculoskeletal System.International journal of molecular sciences · 2026Review
- Mucuna pruriens mitigates aging-related testicular dysfunction and sperm parameters by restoring cell adhesion molecules and junctional complexes.Biogerontology · 2026Article
- Curcumin Between Pleiotropic Potential and Translational Constraints.International journal of molecular sciences · 2026Review
- Inflammation-Driven Remodeling of the Blood-Testis Barrier: Roles of Junctional Complexes, Actin Dynamics, and Kinase Signaling.Biomedicines · 2026Review
- Modulation of mTOR Within Retinal Pigment Epithelium Affects Cell Viability and Mitochondrial Pathology.International journal of molecular sciences · 2025Article
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Authors and funding
11 authors.
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Abstract
The blood-testis barrier (BTB) is composed of tight junctions (TJ) between adjacent Sertoli cells (SCs) and is crucial for sperm growth and development. Aging-induced TJ impairment is closely related to testicular dysfunction. Curcumin, a natural compound, has been widely demonstrated to have a wide range of pharmacological activities, but its regulatory effects on tight junction damage in the testis remain unclear. We here explored the effect of curcumin on TJ function and its underlying molecular mechanism by using D-galactose (D-gal)-induced mouse testis and mouse testicular SCs (TM4) aging models in vitro. In this study, D-gal increased the expression of aging-related proteins p16 and p21, whereas significantly decreased the expression of TJ proteins (ZO-1, Claudin-4, Claudin-7, and Occludin). In addition, curcumin restored the adverse effects of D-gal in the SCs. Autophagy is a degradation system for maintaining cell renewal and homeostasis. D-gal significantly decreased the autophagy level, whereas curcumin restored the effect of D-gal. Using chloroquine (CQ), an inhibitor of autophagy, and rapamycin (RAPA), an activator of autophagy, it was demonstrated that autophagy plays a key role in curcumin amelioration of TJ injury in testicular SCs. Further studies unveiled that autophagy activation was mediated through the AMPK/mTOR pathway. In conclusion, curcumin ameliorates aging-induced TJ damage through AMPK/mTOR signaling pathway-regulated autophagy. This study thus clearly identifies a novel action mechanism of curcumin in the treatment of age-related male reproductive disorders.
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