Achilles tendon (AT) pathologies are common musculoskeletal conditions that can significantly impair function. Despite various traditional treatments, recovery is often slow and may not restore full functionality. The use of extracellular vesicles (EVs) has emerged as a promising therapeutic option due to their role in cell signaling and tissue regeneration. This systematic review aims to consolidate current in vivo animal study findings on the therapeutic effects of EVs on AT injuries. An extensive literature search was conducted using the PubMed, Scopus, and Embase databases for in vivo animal studies examining the effects of EVs on AT pathologies. The extracted variables included but were not limited to the study design, type of EVs used, administration methods, efficacy of treatment, and proposed therapeutic mechanisms. After screening, 18 studies comprising 800 subjects were included. All but one study reported that EVs augmented wound healing processes in the AT. The most proposed mechanisms through which this occurred were gene regulation of the extracellular matrix (ECM), the enhancement of macrophage polarization, and the delivery of therapeutic microRNAs to the injury site. Further research is warranted to not only explore the therapeutic potential of EVs in the context of AT pathologies, but also to establish protocols for their clinical application.

Despite advances in imaging and diagnostics, calcific constrictive pericarditis (CCP) remains a rare and challenging entity, often masquerading as other cardiopulmonary conditions, leading to delayed diagnosis. We present a 70‐year‐old male with a history of heart failure, atrial fibrillation (AF), cirrhosis, chronic obstructive pulmonary disease (COPD), and prior pleural effusion, who was admitted with acute hypoxic respiratory failure and AF with rapid ventricular response (RVR). Imaging revealed extensive pericardial calcifications, leading to a diagnosis of CCP. The patient’s clinical course was marked by refractory hypotension, altered mental status, and progressive cardiohepatic syndrome. Given his high surgical risk, he was managed conservatively and transitioned to palliative care. This case underscores the diagnostic and therapeutic challenges of CCP, particularly in patients with complex comorbidities where surgical intervention is not feasible. It highlights the need for early recognition and individualized management strategies to optimize outcomes in this challenging subset of patients.

Heparan sulfate has many biological activities, in particular positive effects on growth factor signaling and cell adhesion. Thus, mutations in heparan sulfate assembly typically manifest in loss‐of‐function, leading to developmental defects or altered physiology. Here, we demonstrate that genetic and pharmacological reduction of heparan sulfate enhances wound healing, a gain‐of‐function phenotype. In one model, 8‐week‐old mice were shaved and subjected to a full thickness 6‐mm diameter punch biopsy through the dorsal skin. Imaging of the wound over two weeks showed that wound closure occurred more rapidly in mice bearing a defect in Ext gene function, which encodes the copolymerase responsible for the assembly of the backbone of the chain. Enhanced wound closure also occurred after tamoxifen‐induced deficiency of heparan sulfate in skin (Rosa26‐Cre ^ER ; Ext1 ^flox/flox mice) or in keratinocytes (K14‐Cre ^ER ; Ext1 ^flox/fflox ). Wildtype mice treated orally with xyloside also showed significant enhancement in dermal wound repair. We conclude that manipulation of the levels of heparan sulfate in vivo increases the capacity for wound repair, suggesting a novel approach for enhancing the regenerative property of tissues.