Tissue Repair

This narrative review summarizes the current evidence on regenerative peptides relevant to chronic pain management, including collagen peptides, body protection compound-157 (BPC-157), thymosin beta-4 (TB-4), thymosin beta-500 (TB-500), glycyl-L-histidyl-L-lysine copper (GHK-Cu), growth hormone-related peptides, and cibinetide (ARA-290). We review their proposed mechanisms of action, potential clinical applications, preclinical and clinical evidence, safety profiles, and regulatory status. Chronic pain imposes a substantial global burden, yet conventional management strategies often fail to achieve durable, long-term outcomes and primarily focus on symptom control. Regenerative medicine has emerged as a promising alternative by targeting tissue repair and restoration. Among the various therapeutic approaches within regenerative medicine, peptide-based therapies have gained significant attention in recent decades, with growing evidence supporting the efficacy of these interventions. Despite their therapeutic potential, evidence regarding the role of regenerative peptides in chronic pain management remains limited. By synthesizing the available literature, this review aims to provide an evidence-based framework for understanding the potential role of these therapeutic peptides in chronic pain management. However, because most of these therapies remain unapproved by the U.S. Food and Drug Administration (FDA) and clinical evidence in humans is limited, their use should be guided by careful clinical judgment and ongoing evaluation of emerging evidence.

Blood-brain barrier (BBB) repair and angiogenesis after traumatic brain injury (TBI) are pivotal for brain tissue repair. However, the mismatch between the initiation of angiogenesis and BBB integrity may contribute to aggravated edema and neuronal loss. Semaglutide (SEMA) has been validated in both basic and clinical studies for its neuroprotective efficacy against many neurological disorders. However, its intrinsic mechanisms governing BBB repair and angiogenesis remain undefined. A mouse cont

PCSK5 (proprotein convertase subtilisin/kexin 5) is essential for heart development. However, its role in myocardial infarction (MI) remains unexplored. In this study, we found that the plasma levels of PCSK5 were elevated in MI patients and exhibited potential in predicting cardiac function improvement. PCSK5 expression was upregulated in cardiac endothelial cells (ECs) of MI patients. Pcsk5 deficiency in ECs impaired angiogenesis and cardiac recovery post-MI, and delayed tissue repair followin

After injury, the repair of brain tissue is hindered by poor neuronal regeneration and severe neuroinflammation. Although magnetoelectric (ME) stimulation has emerged as a promising wireless strategy to promote axonal growth, its efficacy is strictly dependent on the ME coupling efficiency of the materials used. Furthermore, while microglia-mediated inflammation remains a critical barrier to neurogenesis, integrating neuroprotective strategies to modulate this inhibitory environment with ME stim

Diabetic wounds struggle to heal because of ROS-mediated immune dysfunction, in which the mitochondrial metabolic reprogramming of macrophages is critical for inflammation resolution and tissue repair. Here, we innovatively combine the antioxidant astaxanthin (Ast) and the metabolic activator metformin (Met) via pH-responsive dynamic Schiff base linkages to form amphiphilic Ast-PEG-Met conjugates, which self-assemble into nanomicelles (NMs). This strategy effectively improves the solubility of A

Diabetic foot ulcer (DFU) is characterized by persistent inflammation, metabolic dysfunction, and impaired angiogenesis, leading to refractory chronic wounds. Here, we report an adhesive, metformin-loaded (1.0 mM) polyethylene glycol (PEG) based hydrogel (i.e., PEG/Met), constructed from equal volume of PEG-SG (20 wt.%) and PEG-NH2 (20 wt.%), to regulate macrophage polarization and metabolism in DFU. Density functional theory (DFT) calculations and infrared spectrum confirmed its crosslinking, y