CTSK (Cathepsin K)

MMP13 may promote aggressive behavior in chordoma by degrading growth-inhibitory COL2-rich ECM. These data support MMP13 as a potential unfavorable prognostic marker and therapeutic target in chordoma.

NF-ϰB inhibitor treatment significantly decreased the above mRNA levels both in serum and joint tissues. NF-ϰB pathway inhibition can ameliorate bone destruction in the foot joints of CIA mice, which may be related to the reduction of inflammatory bone destruction and osteoclastogenesis.

Poor solubility, systemic toxicity, and therapeutic resistance hamper conventional approaches, such as docetaxel (Dtx) treatment... Our intratibial bone mCRPC mouse model provides a robust platform for studying PCa bone metastases and evaluating nanomedicine efficacy. PGA-Dtx displays promise as a safe and effective therapy for mCRPC, offering improved drug delivery and reduced systemic side effects, which supports the translational potential of polymer-drug conjugates in mCRPC management.

Our findings demonstrate that γ-Mag inhibits osteoclastogenesis and bone resorption by targeting the PI3K/AKT/NF-κB pathway, thereby blunting the C-FOS/NFATc1 transcriptional program. This study establishes γ-Mag as a promising natural lead compound for the treatment of postmenopausal osteoporosis.

These findings demonstrate the dose-dependent inhibitory effect of L-quebrachitol on osteoclastogenesis through the modulation of RANK-mediated signaling pathways and prevention of bone loss in an animal model. However, further exploration of the potential of L-quebrachitol as an effective approach for osteoporosis is required.

Ferritin and RANKL synergistically promote monocyte osteoclastogenesis, driving alveolar bone resorption in periodontitis. Targeting ferritin signaling may offer therapeutic potential to mitigate bone loss.

We found that cathepsin K (CTSK) uniquely degrades cell-surface mucins, proteoglycans, and polysialylated glycoproteins, and we demonstrated that cathepsin K reduces total glycocalyx thickness. These findings establish CTSK as a promising starting point for the development of a glycocalyx-debulking enzyme for cancer therapeutics.

These results suggest that local administration of MR16-1 may enhance CGRP expression, promote callus maturation, and accelerate fracture healing, indicating a potential role in bone repair.

Additionally, this review examines the interplay among molecular mechanisms that regulate osteoclast differentiation and activation under pathological and inflammatory conditions, elucidates their roles in osteoclast hyperactivation-related human diseases, and provides a comprehensive framework for understanding these processes. Finally, it underscores potential novel therapeutic strategies for osteoclast-related skeletal lytic diseases and highlights perspectives for future investigations.

In TFE3-rearranged RCC, the fusion gene might influence morphology or PD-L1 expression, thereby be likely to affect the efficacy of immunotherapy. Assessment of a combination of histological morphology, immunophenotype, and genetic alterations can facilitate precise pathological diagnosis of RCC, supporting personalized targeted therapy and prognosis assessment.

After 12 days, the (D-Ala2)GIP-treated group showed significantly reduced tooth movement and fewer osteoclasts and odontoclasts on the compression side compared to the PBS control. These findings suggest that (D-Ala2)GIP inhibits OTM, potentially by suppressing TNF-α-driven osteoclastogenesis and bone resorption.

In conclusion, p21 deficiency exacerbates bone destruction in arthritis by promoting osteoclast differentiation and inflammatory cytokine expression via the IL-6/STAT3 pathway. Targeting p21 may offer therapeutic potential for preventing arthritis-related bone loss, such as in RA.