Microsecond molecular dynamics simulations reveal how Cathepsin K unwinds tropocollagen with chondroitin 4-sulphate, indicating potential for inhibitor design.
Cathepsin K (CatK), a promising therapeutic target for bone-related diseases, uniquely unfolds triple-helical collagen and digests tropocollagen into soluble peptides in the presence of chondroitin 4-sulphate (C4-S). However, the molecular mechanism of CatK-mediated collagenolysis remains poorly understood, hindering the rational design of selective inhibitors. In this study, we performed microsecond-scale molecular dynamics simulations of a fully solvated ternary complex comprising the CatK dimer, tropocollagen segment, and C4-S, to indicate the structural and dynamical basis of tropocollagen unwinding. The process was initiated by the progressive disruption of six key inter-chain hydrogen bonds within the tropocollagen. C4-S adopted a cosine-like conformation that bridged CatK and tropocollagen, thereby stabilising the ternary complex. Unwinding occurred at the active site cleft, with Cys25 and Trp184 serving as critical residues that may contribute hydrogen bond disruption and substrate stabilisation. Our findings provided mechanistic insights into CatK-dependent collagen degradation and rational development of next-generation CatK inhibitors.
No takes yet. Share an insight, caveat, or question.
Shan et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: