Eucalyptus grandis (E. grandis) has been reported to form a symbiosis with arbuscular mycorrhizal fungi (AMF), which plays an important role in improving plant tolerance of heavy metal. However, the mechanism of how AMF intercept and transport cadmium (Cd) at the subcellular level in E. grandis still remains to be researched. In this study, a pot experiment was conducted to investigate the growth performance of E. grandis under Cd stress and Cd absorption resistance of AMF and explored the Cd localization in the root by using transmission electron microscopy and energy dispersive X-ray spectroscopy. The results showed that AMF colonization could enhance plant growth and photosynthetic efficiency of E. grandis and reduce the translocation factor of Cd under Cd stress. After being treated with 50, 150, 300, and 500 μM Cd, the translocation factor of Cd in E. grandis with AMF colonization decreased by 56.41%, 62.89%, 66.67%, and 42.79%, respectively. However, the mycorrhizal efficiency was significant only at low Cd concentrations (50, 150, and 300 μM). Under 500 μM Cd concentration condition, the colonization of AMF in roots decreased, and the alleviating effect of AMF was not significant. Ultrastructural observations showed that Cd is abundant in regular lumps and strips in the cross-section of E. grandis root cell. AMF protected plant cells by retaining Cd in the fungal structure. Our results suggested that AMF alleviated Cd toxicity by regulating plant physiology and altering the distribution of Cd in different cell sites.

Osteoarthritis (OA) has evolved from a condition conventionally regarded as mere mechanical “wear and tear” to a complex, whole-joint disorder driven by chronic low-grade inflammation and cellular dysfunction. Within the joint, the osteoimmune microenvironment—composed of articular cartilage, synovium, subchondral bone, the infrapatellar fat pad (IPFP), and resident stem cell niches—serves as the central site of osteoimmune interaction for maintaining tissue homeostasis and repair. Accumulating evidence indicates that age-associated dysregulation and senescence of innate and adaptive immune cell subsets represent major contributors to OA progression. Age- and senescence-associated immune states generate persistent inflammatory, oxidative, and damage-associated signals that contribute to microenvironmental deterioration. In this review, we propose a unified framework elucidating how immunosenescence reshapes the osteoimmune microenvironment via aberrant intercellular communication. We systematically delineate the distinct cellular crosstalk networks connecting immunosenescent drivers with chondrocytes, synovial fibroblasts, subchondral bone remodeling units, IPFP adipocytes, and mesenchymal stem/stromal cells (MSCs). Furthermore, we highlight emerging therapeutic avenues to reprogram this senescent niche, encompassing senotherapeutics, immunometabolic reprogramming, biomaterial-assisted targeted delivery, and engineered cell therapies. Finally, we propose the “Resolution Failure Hypothesis” as a testable mechanistic framework in which impaired efferocytosis and dysregulated specialized pro-resolving mediator (SPM) signaling may contribute to the persistence of osteoimmune remodeling. Rather than proposing defective inflammation resolution as a new biological phenomenon, this framework integrates established resolution-related mechanisms with age-associated immune remodeling and asks whether insufficient restoration of clearance and resolution capacity helps explain the incomplete structural recovery observed after senescent-cell-targeted interventions. Reconceptualizing OA through the lens of immunosenescent crosstalk will accelerate the translation of disease-modifying therapies from microenvironmental modulation toward functional joint regeneration.