Primary cilium–mediated mechanotransduction in cartilage chondrocytes

Abstract

Osteoarthritis (OA) is one of the most prevalent joint disorders associated with the degradation of articular cartilage and an abnormal mechanical microenvironment. Mechanical stimuli, including compression, shear stress, stretching strain, osmotic challenge, and the physical properties of the matrix microenvironment, play pivotal roles in the tissue homeostasis of articular cartilage. The primary cilium, as a mechanosensory and chemosensory organelle, is important for detecting and transmitting both mechanical and biochemical signals in chondrocytes within the matrix microenvironment. Growing evidence indicates that primary cilia are critical for chondrocytes signaling transduction and the matrix homeostasis of articular cartilage. Furthermore, the ability of primary cilium to regulate cellular signaling is dynamic and dependent on the cellular matrix microenvironment. In the current review, we aim to elucidate the key mechanisms by which primary cilia mediate chondrocytes sensing and responding to the matrix mechanical microenvironment. This might have potential therapeutic applications in injuries and OA-associated degeneration of articular cartilage.

Structure, function, and research progress of primary cilia in reproductive physiology and reproductive diseases

“…Disruptions in the signaling pathways of primary cilia may result in developmental and physiological deficiencies within the organism (Ma et al, 2022). Primary cilia, serving as antennae, have the capability to sense the cellular microenvironment and play a pivotal role in mediating the signal transduction of diverse signaling pathways (Zhang et al, 2023). Within primary cilia resides a highly conserved bidirectional transport system known as the Intra-Flagellar Transport (IFT) system, initially identified in Chlamydomonas (Prevo et al, 2017).…”

PDZK1 protects against mechanical overload-induced chondrocyte senescence and osteoarthritis by targeting mitochondrial function

“… 7 However, the molecular and cellular mechanisms that underlie the transduction of physical signals to biochemical signals resulting in OA progression have not been fully elucidated. 8 – 10 Mitochondria, which are membrane-enclosed organelles and produce cellular energy in the form of adenosine 11 triphosphate (ATP), are currently a focus of biomedical research because of their role in aging and the development of OA pathologies. 12 , 13 Growing evidence suggests that mitochondrial dysfunction not only leads to cellular senescence, but also accelerates organismal aging via mechanisms associated with mitochondrial reactive oxygen species (ROS) production, mitochondria DNA (mtDNA) mutations and mitochondrial biogenesis.…”