Mitophagy is an essential mechanism in maintaining cellular homeostasis, in which damaged and superfluous mitochondria are selectively degraded by the autophagy-lysosome pathway. Our recent study revealed that SPATA33 functions as a novel receptor for mitophagy in the priming of mitochondria for degradation in male germline cells. SPATA33 directly mediates the interaction of the outer mitochondrial membrane protein VDAC2 with the autophagy machinery component ATG16L1 during mitophagy. Upon starvation induction, SPATA33 can promote mitophagy as an autophagy receptor. Thus, SPATA33 confers cargo selectivity during mitophagy in germline cells. These findings provide new insights into selective autophagy and mitochondrial homeostasis.

Coat color is a crucial production trait for fur-bearing animals and significantly influences their economic value. The remarkable diversity of coat colors in rex rabbits not only provides a wide range of market options but also serves as an essential resource for investigating the genetic mechanisms underlying coat color formation. In this study, we conducted integrated transcriptomic and proteomic profiling of skin tissues from black and white Rex Rabbits, revealing the presence of 52 co-expressed genes/proteins. Proteomic analysis revealed a significant upregulation of PMEL (p = 0.030, FC = 2.194), while transcriptomic data indicated an even more pronounced upregulation (p = 0.028, FC = 35.279). Therefore, PMEL (Premelanosome Protein) may serve as a pivotal regulator of melanogenesis in Rex Rabbits. Our findings indicate that PMEL overexpression in melanocytes increases melanin content, promotes melanocyte proliferation, and enhances the expression of melanin-related genes (MITF, TYR, TYRP1, and GPNMB) while inhibiting melanocyte apoptosis. Conversely, PMEL knockdown significantly reduces melanin content, melanocyte proliferation, and the expression of melanin-related genes while promoting melanocyte apoptosis. These findings suggest that PMEL contributes to melanogenesis in Rex Rabbits.

To investigate the clinical pathways via which the glaucomatous optic nerve damage (GOND) occurred in cases with glaucomatocyclitic crisis (also called Posner-Schlossman syndrome, PSS). A retrospective study was conducted, 59 PSS patients with confirmed GOND were screened out from 190 PSS cases and followed up for a period of 5 ± 3.3 years. Clinical data were retrospectively analyzed systematically and dynamically, including intraocular pressure and its dynamic change, appearance of fundus, visual field and the state of anterior chamber angle in initial and later period during the episodes and intermission of PSS. Based on the clinical data, a classification and standard for the clinical pathways of GOND were established, and the clinical pathway of GOND in each patient was classified accordingly. There are at least 4 clinical pathways of GOND in PSS patients, namely: Type A: GOND was simply caused by the accumulation effect of high IOP during many attacks of PSS itself. Type B: GOND was resulted from the combined action of PSS itself and another type of secondary open-angle glaucoma. The recurrent inflammation during the episodes of PSS damaged the trabecular meshwork, which can cause elevation of IOP during the intermission of PSS. Type C: PSS combined with primary open angle glaucoma (POAG). Type D: PSS combined with primary angle-closure glaucoma (PACG). Base on the clinical gateways of GOND classification above, the cases of type A, B, C, and D were 27, 6, 19, and 7 respectively. The staging of visual field damage in cases with GOND from different clinical pathways showed a significant difference (Person chi-square χ² test, χ² = 7.211, P = .007). There are at least 4 clinical pathways of GOND in PSS patients, and each clinical pathway corresponds to different clinical features and different treatment principles. It is extremely important to correctly discriminate the pathways of GOND in PSS patients.

The regeneration and repair of scarless skin tissue remain a significant challenge for full-thickness wounds. Traditional wound management approaches, particularly passive healing through scabbing and conventional mechanical debridement, are frequently associated with significant pain, high infection risks, and abnormal scar formation, often failing to support the regeneration of skin appendages like hair follicles. In recent years, collagen-based scaffolds have been widely adopted in tissue-engineered skin substitutes owing to their favorable biocompatibility. However, their simplistic, single-component architecture inherently lacks the dynamic, cell-instructive microenvironment found in native skin, which not only compromises the long-term survival and functional integration of seeded cells but also directly leads to insufficient reconstruction of the dermo-epidermal junction, thereby impairing skin barrier function and ultimately limiting overall regenerative efficacy. In this study, we propose a biomimetic multilayer composite scaffold system in which decellularized amniotic membrane matrix (AM) is combined with fibroblast-laden collagen gel (FCG) and seeded with epidermal stem cells (EpiSCs). This bionic skin (denoted as AM-FCG-EpiSCs) is designed to achieve hierarchical regeneration of full-thickness skin defects. Compared with injured skin treated with Moropicin ointment, the injured skin treated with AM-FCG-EpiSCs healed more quickly and regenerated appendages like hair follicles without scarring. The results show that the biomimetic structure of AM-FCG-EpiSCs can mediate dynamic cell–cell interactions and regulate the microenvironment. This breakthrough overcomes the dual challenges of scar suppression and functional restoration in full-thickness skin regeneration, offering an innovative solution for translational medicine.