The elderly suffer from a higher incidence and greater severity of acute kidney injury (AKI), yet the underlying molecular mechanisms remain poorly understood. This study dissects the possible role of thousand and one amino acid protein kinase 1 (TAOK1) in age-related AKI, specifically examining its regulation of mitophagy. Aged (23~24 months) C57BL/6 mice were subjected to renal ischemia-reperfusion injury (IRI) and TAOK1 was overexpressed in these mice. Renal function, histopathology, inflammation, neutrophil extracellular trap (NET) formation, and fibrosis were assessed. The involvement of the STK3/BNIP3 pathway and mitophagy was evaluated by Western blot and immunofluorescence. In vitro, primary renal tubular cells from aged mice underwent hypoxia-reoxygenation (H/R) following Taok1 knockdown. TAOK1 expression was significantly downregulated in the kidneys of aged mice. Taok1 overexpression in aged mice ameliorated IRI-induced renal dysfunction, tubular damage, inflammation, NET formation, and fibrosis. Mechanistically, Taok1 overexpression activated the STK3/BNIP3 signaling pathway and enhanced mitophagy, as evidenced by increased expressions of key mitophagy-related proteins. Conversely, Taok1 knockdown in aged mouse renal tubular cells exacerbated H/R-induced cell injury and apoptosis, and suppressed the STK3/BNIP3 pathway and mitophagy. Our findings demonstrate that TAOK1 protects against renal IRI in aged mice by promoting mitophagy through the STK3/BNIP3 axis. The age-related decline in TAOK1 may contribute to the heightened susceptibility to AKI, positioning TAOK1 as a potential therapeutic target for mitigating AKI in the aging population.
Addressing hair damage is essential for maintaining overall hair and scalp health. Previous studies have suggested that low-molecular-weight collagen peptides may support hair follicle biology through regulation of extracellular matrix homeostasis and cellular signaling pathways. In addition, recent preclinical studies have demonstrated that low-molecular-weight fish collagen peptides promote hair regrowth through activation of proliferative signaling and suppression of inhibitory pathways. However, their clinical efficacy in improving hair damage has not been clearly established. In this study, the efficacy and safety of low-molecular-weight collagen peptide GT (LMWCP GT) were evaluated in Korean adults with damaged hair. In a randomized, placebo-controlled trial, individuals aged 19∼60 years without alopecia but with mild to moderate hair damage received LMWCP GT (3 g/day) for 24 weeks. Compared with placebo, the treatment group demonstrated significant improvements in hair gloss, as measured using a gloss meter (SAMBA) and scanning electron microscopy, as well as in hair elasticity, assessed by tensile strength and hair diameter. Subjective evaluations further indicated improvements in overall hair condition, including gloss, elasticity, thickness, texture, fullness, and appearance. In addition, scalp elasticity was significantly increased in the treatment group. No treatment-related adverse events were observed. These findings indicate that daily supplementation with LMWCP GT (3 g/day) for 24 weeks is safe and effective in improving overall hair condition in individuals with damaged hair without alopecia.
The clinical application of mesenchymal stem cells (MSCs) has several limitations owing to their less therapeutic efficacy. Effect enhancement and MSCs from new sources might help in overcoming these limitations. The aim of the present study was to investigate the therapeutic effects of human Wharton's jelly-derived MSCs (hWJMSCs) and pioglitazone-pretreated MSCs (Pio-MSCs) in a rat tendon injury model. Fifty-four Sprague Dawley rats were randomly assigned to three groups: phosphate-buffered saline (PBS) group, implanted with PBS; MSC group, implanted with MSCs; and Pio-MSC group, implanted with Pio-MSCs. The cell or PBS with fibrin glue mixture was implanted around bilateral window defect in the Achilles tendons of the rats. The cross-sectional area measurement, histological analysis, gene expression, protein expression, and biomechanical analysis were performed at 2 and 4 weeks after modeling. Pio-MSC group revealed a significantly higher gene expression level of Col3 than PBS group at 2 weeks and that of TnC at 2 and 4 weeks. Moreover, MSC group revealed significantly higher gene expression level of Col1 than PBS group at 2 weeks. In general, the expression levels of Col1, Col3, Scx, and TnC were the highest in Pio-MSC group, followed by MSC and PBS groups. Furthermore, Pio-MSC group revealed significantly higher tenascin C-stained fraction than PBS group at 4 weeks. These findings suggest a potential role of hWJMSCs in tendon regeneration; however, the in vivo enhancement effect of pioglitazone pretreatment over MSC alone was not confirmed, and no differences were observed in histological or biomechanical outcomes among the groups.
As human longevity continues to increase globally, the prevalence of age-related deterioration and associated chronic lung diseases has risen in parallel. Unlike many organs, the lung is continuously exposed to environmental insults, leading to cumulative cellular damage, impaired epithelial progenitor activity, and chronic inflammation, which contribute to diseases such as pulmonary fibrosis and chronic obstructive pulmonary disease. Under physiological conditions, lung homeostasis is maintained by epithelial progenitor cells, particularly alveolar type II cells. However, this regenerative capacity is often disrupted in chronic lung diseases, resulting in impaired repair and fibrotic remodeling. Fibroblast growth factors (FGFs) and their receptors (FGFRs) play critical roles in epithelial regeneration, cell survival, and tissue repair. Despite their therapeutic potential, clinical translation remains limited by poor protein stability, rapid proteolytic degradation, low delivery efficiency across biological barriers, and insufficient cell-type specificity due to broad FGFR expression. Recently, several delivery strategies have been evaluated in preclinical lung disease models, including protein engineering, nanoparticle and liposome-based platforms, protein transduction domain- and cell-penetrating peptide-based intracellular delivery, and mesenchymal stem cell-based approaches. Therefore, this review summarizes the roles of FGF signaling in lung regeneration and age-associated diseases, and discusses emerging delivery strategies aimed at bridging the gap between preclinical efficacy and clinical application.
Pericytes are mural cells embedded within the microvascular wall that regulate endothelial stabilization, angiogenesis, and vascular permeability. Once regarded as a relatively uniform vascular support population, pericytes are now recognized as quantitatively and functionally heterogeneous across organs. Neural barrier beds such as brain and retina exhibit high pericyte density and near-continuous mural coverage, whereas peripheral tissues including skeletal muscle display sparse investment. These anatomical differences parallel functional specialization, with central nervous system pericytes exerting strong control over blood-brain barrier (BBB) integrity and transcytosis, while peripheral pericytes participate prominently in vascular remodeling and repair. A critical yet under-integrated dimension of this heterogeneity is developmental origin. Trunk and visceral pericytes arise predominantly from mesodermal progenitors, whereas cranial and forebrain-associated pericytes derive largely from neural crest lineage. This spatial segregation of embryonic origin aligns with vascular specialization, suggesting that lineage contributes to mural regulatory architecture. Stem cell-based comparisons further demonstrate that neural crest-derived pericyte-like cells induce BBB phenotypes more effectively than mesoderm-derived counterparts under identical endothelial conditions, supporting a lineage-linked functional bias. This review integrates anatomical distribution, quantitative investment patterns, molecular signaling mechanisms, and embryonic lineage into a unified framework of pericyte heterogeneity. We propose that developmental origin establishes a regulatory foundation upon which vascular niche signals act, and should therefore be treated as a primary experimental and translational design variable in vascular modeling and regenerative strategies.
