Role of myocardium-derived exosomal miRNAs in doxorubicin-induced cardiomyopathy.

Isochlorogenic acid A ameliorates atopic dermatitis by modulating JAK/STAT3, NF-κB, and MAPK pathways in a DNFB/PM2.5-induced mouse model.

Structural characterization of Auricularia cornea 'Yumuer' polysaccharides and their alleviation of allergic asthma in mice via gut microbiota modulation.

Isolation, characterization, and anti-neuroinflammatory activity of sesquiterpenoids from Pogostemon esquirolii.

Sennoside A ameliorates cognitive impairment by inhibiting USP14/ERK1/2 pathway in a mouse model of type 2 diabetes mellitus.

USP7 inhibition promotes wound healing by suppressing M1 macrophage polarization via NF-κB/MAPK signaling pathway.

Quanzhenyiqitang and its polysaccharides alleviate chronic obstructive pulmonary disease inflammatory injury through TLR4/MyD88/MAPK signaling pathway.

Rationale: Natural killer (NK) cells are emerging as a promising source of immunomodulatory secretomes with regenerative potential. However, heterogeneity in primary NK cell populations limits the reproducibility of NK-derived cell-free therapies. To address this, we developed directly reprogrammed NK (drNK) cells with a stable CD56brightCD16bright phenotype and investigated the therapeutic potential of their conditioned medium (drNK-CM) in wound healing, focusing on underlying molecular mechanisms such as chemokine signaling and angiogenesis. Methods: drNK cells were generated by transcription factor-mediated reprogramming (OCT4, SOX2, KLF4, MYC) and characterized via flow cytometry and RNA-seq. The secretome profile of drNK-CM was evaluated using proteomic analysis. Human epidermal keratinocytes (HEKs), dermal fibroblasts (HDFs), and endothelial cells (HUVECs) were treated with drNK-CM to assess proliferation, migration, and extracellular matrix (ECM) remodeling. Chemokine receptor involvement was evaluated using CCR1, CCR3, and CCR5 antagonists. In vivo efficacy was tested in mouse excisional wound models, with histological and immunofluorescence evaluation of angiogenesis, re-epithelialization, and collagen deposition. Results: drNK-CM significantly promoted proliferation and migration of HEKs, HDFs, and HUVECs, accompanied by enhanced expression of Type I/III collagen, VEGF, and MMPs. Transcriptomic profiling revealed that drNKs uniquely upregulated genes associated with ECM remodeling, chemokine signaling (CCL3/4/5), and angiogenesis. Notably, CCR5 inhibition by maraviroc abrogated drNK-CM-induced cell migration and delayed wound closure in vivo, highlighting the central role of the CCL3/4/5-CCR5 axis. Furthermore, drNK-CM activated AKT and ERK pathways and promoted anti-inflammatory macrophage polarization. In vivo application of drNK-CM accelerated wound closure, improved neovascularization, and supported organized tissue regeneration compared to controls. Conclusion: This study demonstrates that drNK-CM enhances wound healing through coordinated actions on epithelial, stromal, and endothelial compartments. The reparative effects are primarily mediated via the CCL3/4/5-CCR5 signaling axis and pro-angiogenic cascades. Given their consistent phenotype and reproducible secretome, drNKs represent a scalable and safe source for cell-free regenerative therapeutics.

Anti-colitic effects of Centella asiatica (L.) Urb. juice via ERK/p38 and NF-κB signaling modulation and the characterization of a key marker compound.

Transcriptome analysis of Crandell Rees Feline Kidney (CRFK) cells infected with Feline calicivirus strain 023 (FCV 023).

Escitalopram disrupts PDK1-Akt signaling in B cells through a structure-dependent mechanism independent of SERT.

Red nucleus IL-15 facilitates the development of neuropathic pain in male rats by inducing inflammatory factors: implying the involvement of NF-κB and p38 MAPK.

CircP4HA3/miR-5001-5p/THBS2 axis promotes chondrocyte senescence and cartilage degradation during osteoarthritis progression.

Metabolic reprogramming represents a targetable mechanism to overcome acquired resistance to venetoclax in acute myeloid leukemia.

Curzerenone attenuates neuroinflammation and oxidative stress via MAPK signaling pathway modulation: Network pharmacology and in vivo insights in a scopolamine-induced model of Alzheimer's disease

Protective effect of liquiritin against cisplatin-induced liver injury in mice through reduction of inflammation, oxidative stress, apoptosis and inhibition of p38 MAPK/p53 pathway based on network pharmacology and in experimental validation.

Effect of amyloid-beta 1-40 and 1-42 peptides on the lateral diffusion and signaling of receptor for advanced glycation endproducts (RAGE).

Huayu Xiaopi Decoction regulates the JNK/c-Jun/Slug pathway to inhibit epithelial-mesenchymal transformation and improve precancerous lesions of gastric cancer.

NIR/US-responsive injectable hyaluronic acid-based nickel sulfide hydrogel as a smart platform for synergistic antitumor therapy.

Shenkang (SK) is a widely used formula for treating chronic kidney disease (CKD) since the 1990s. However, the associations of SK use with the long-term outcome among CKD patients have not been validated in real‐world study. This single-center retrospective study included outpatients with CKD from 1 January 2013, to 31 December 2023. Patients who received SK were compared with control group after propensity score matching. A total of 2,463 patients met the inclusion criteria, with 546 matched pairs. The SK group had a significantly lower risk of end-stage renal disease (adjusted hazard ratios = 0.83, 95% confidence interval: 0.70–0.98; p = 0.030), and the cumulative event of end-stage renal disease was significantly lower in the SK group than in the control group (p = 0.027). The estimated glomerular fitration decline in SK group was also significantly slower than those in control group (p < 0.001). Subgroup analysis showed that SK had significant benefit in male patient. Network pharmacology was used to explore underlying mechanisms, which indicated that SK targets are enriched in epithelial cell proliferation, fluid shear stress, P13K-Akt, and MAPK signaling pathways. In summary, SK is a promising therapeutic option for improving clinical outcomes in CKD, potentially mediated by modulating the PI3K/AKT and MAPK signaling pathways, and modulating hemodynamics. However, further experimental validation both in vivo and in vitro is required.