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An autonomous bioelectronic suture that programs tendon regeneration through endogenous electromechanical-cues

ABSTRACT: Tendon injuries disrupt the physiological equilibrium between mechanical stability and joint mobility, often resulting in persistent functional impairment. The regeneration of tendons with mature architecture and full biomechanical functionality remains a pivotal challenge in current clinical treatment and tissue repair. Here we introduce a self-powered, biomimetic electronic suture (BSE-suture) that converts physiological motion into adaptive bioelectrical and cellular regulation for accelerated tendon regeneration. The platform integrates a hierarchically organized architecture with a stem cell-laden hydrogel interface, enabling simultaneous mechanical compliance, autonomous electromechanical transduction, and local biological control. The suture matches the tensile performance of clinical sutures while minimizing interfacial friction and maintaining robust structural integrity. Under tendon-relevant deformation, it generates stable electrical outputs (~4 V, ~110 mV mm⁻¹) without external power sources. This self-generated stimulation preserves stem cell viability, directs tenogenic fate commitment and enhances regenerative signaling. In a rat Achilles tendon defect model, the SBE-suture markedly improved collagen organization, promoted functional tissue remodelling, and restored locomotor performance. The platform further reshapes the immune microenvironment by biasing macrophage polarization toward a reparative phenotype. By transforming sutures from passive mechanical fixators into active bioelectronic regulators, this work introduces a new class of self-adaptive regenerative implants that dynamically couple biomechanics with tissue regeneration in mechanically active organs.

ORGANISM(S): Rattus Norvegicus

SUBMITTER: Yuqi Zhang

PROVIDER: PXD078537 | iProX | Mon May 18 00:00:00 BST 2026

REPOSITORIES: iProX

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Project description:The myotendinous junction (MTJ) is a critical interface connecting skeletal muscle and tendon, responsible for transmitting contractile forces and ultimately enabling musculoskeletal movement. Due to its complex architecture, the MTJ is particularly susceptible to injury under conditions of excessive stretching, high-impact loading, aging and neuromuscular disorders such as muscular dystrophies. Despite its significant physiological role, research on the MTJ remains limited, primarily due to the challenges associated with obtaining human tissue samples. This limitation underscores the urgent need for advanced in vitro models that can accurately replicate tissue-specific features. In this work, we developed a human-derived 3D MTJ-like model using the rotary wet-spinning (RoWS) technology. Human primary pericytes (hPeri) and human tendon derived stem cells (hTDSC) were spatially patterned within the extruded hydrogel fibers in a consecutive manner to form highly integrated and anisotropically aligned biomimetic multicellular tissue constructs. Upon maturation, immunofluorescence analysis confirmed the presence of tendon and muscle-tissue specific markers including Collagen type I (COL1), Collagen type III (COL3), Tenascin (TNC), Tenomodulin (TNMD) and Myosin Heavy Chain (MHC), respectively. Specifically, cellular organization recapitulated the interdigitated architecture typical of the MTJ native microenvironment. Moreover, the expression of Collagen type VI (COL6), Thrombospondin 4 (THSB4), and Collagen type XXII (COLL22A1), along with the polarized localization of Paxillin (PXN) and Neural Cell Adhesion Molecule 1 (NCAM1) at the myotube–tendon interface, confirmed the establishment of a highly specialized junctional niche characterized by active cell–matrix interactions and cytoskeletal anchorage. Notably, Dystrophin expression was detected both in tendon and MTJ-like constructs, suggesting a novel potential target for the investigation of MTJ degeneration in muscular dystrophies condition. Collectively, our biomimetic 3D model could offer a promising platform for the in-depth investigation of musculoskeletal development, pathophysiological processes, and the advancement of targeted therapeutic strategies.

Project description:Variability of regenerative potential among animals has long perplexed biologists. Based on their amazing regenerative abilities, planarians have become important models for understanding the molecular basis of regeneration; however, planarian species with limited regenerative abilities are also found. Despite the importance of understanding the differences between closely related, regenerating and non-regenerating organisms, few studies have focused on the evolutionary loss of regeneration, and the molecular mechanisms leading to such regenerative loss remain obscure. Here we examine Procotyla fluviatilis, a planarian with restricted ability to replace missing tissues, utilizing next-generation sequencing to define the gene expression programs active in regeneration-permissive and regeneration-deficient tissues. We found that Wnt signaling is aberrantly activated in regeneration-deficient tissues. Remarkably, down-regulation of canonical Wnt signaling in regeneration-deficient regions restores regenerative abilities: blastemas form and new heads regenerate in tissues that normally never regenerate. This work reveals that manipulating a single signaling pathway can reverse the evolutionary loss of regenerative potential. RNA-seq experiments to identify gene expression changes following amputation in body regions with variable regenerative potential. Adult Procotyla fluviatilis were amputated at sites either anterior or posterior to the pharynx. After 24 hours post-amputation, tissues near the amputation site were excised and RNA was extracted. Similar tissues were excised from uncut control animals. Samples were processed for RNA-seq using Illumina procedures. We generated a de novo P. fluviatilis transcriptome and used RNA sequencing (RNA-seq) to characterize transcripts from excised tissue fragments in Reg+ and Reg- body regions 24 hours post-amputation. We performed parallel analyses on tissues excised from intact animals at identical body regions to account for regional differences in transcripts, thereby identifying changes resulting from amputation. Samples A1-A3 = Regeneration-proficient (Reg+) tissue excision 24 hours after amputation. Samples B1-B3 = Tissue excision from regeneration-proficient (Reg+) region but not amputated. Samples C1-C3 = Tissue excision from regeneration-deficient (Reg-) tissues 24 hours after amputation. Samples D1, D3-D4 = Tissue excision from regeneration-deficient (Reg-) region that was not amputated.

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An autonomous bioelectronic suture that programs tendon regeneration through endogenous electromechanical-cues

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