Exosomes are small extracellular vesicles released by a range of cells, including mesenchymal stromal/stem cells (MSCs), immune cells, cancerous cells, etc. These particles contain biomolecules such as DNA, microRNA, messenger RNA, protein, and lipid, and play a vital role in establishing cellular communication. After reaching the target cells, the particles cause changes in function, fate, morphology, differentiation, and growth. Exosomes released from a variety of sources have the ability to influence the behavior of cells involved in wound healing, enhance neovascularization, promote collagen deposition, reduce inflammation, and quicken the healing process. According to new research, endothelial cell adhesion, migration, proliferation, vascular repair, and angiogenesis are all accelerated during the wound healing process when deleted in malignant brain tumors 1 (DMBT1) is used as an active stimulant. This article will review DMBT1 protein as one of the major elements of exosomes from human urine-derived MSCs.

Various factors can influence the complex process of wound healing. Non-coding RNAs (ncRNAs), which include long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), as well as microRNAs (miRNAs), contribute critically to the regulation of wound healing mechanisms. Specific miRNAs regulate fibroblast proliferation, migration, and extracellular matrix production, while others influence keratinocyte migration and re-epithelialization. Some miRNAs also modulate the inflammatory response and regulate angiogenesis during wound healing. The emerging significance of circRNAs in regulating fibroblast and keratinocyte functions during wound healing are also to be noted, as are the significant roles lncRNAs play in influencing various aspects of wound healing. This review underscores the pivotal roles played by ncRNAs in orchestrating the intricate processes involved in wound healing, providing insights into potential therapeutic targets and strategies for enhancing wound healing outcomes.

Exosomes are small extracellular vesicles released by a range of cells, including mesenchymal stromal/stem cells (MSCs), immune cells, cancerous cells, etc. These particles contain biomolecules such as DNA, microRNA, messenger RNA, protein, and lipid, and play a vital role in establishing cellular communication. After reaching the target cells, the particles cause changes in function, fate, morphology, differentiation, and growth. Exosomes released from a variety of sources have the ability to influence the behavior of cells involved in wound healing, enhance neovascularization, promote collagen deposition, reduce inflammation, and quicken the healing process. According to new research, endothelial cell adhesion, migration, proliferation, vascular repair, and angiogenesis are all accelerated during the wound healing process when deleted in malignant brain tumors 1 (DMBT1) is used as an active stimulant. This article will review DMBT1 protein as one of the major elements of exosomes from human urine-derived MSCs.

Various factors can influence the complex process of wound healing. Non-coding RNAs (ncRNAs), which include long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), as well as microRNAs (miRNAs), contribute critically to the regulation of wound healing mechanisms. Specific miRNAs regulate fibroblast proliferation, migration, and extracellular matrix production, while others influence keratinocyte migration and re-epithelialization. Some miRNAs also modulate the inflammatory response and regulate angiogenesis during wound healing. The emerging significance of circRNAs in regulating fibroblast and keratinocyte functions during wound healing are also to be noted, as are the significant roles lncRNAs play in influencing various aspects of wound healing. This review underscores the pivotal roles played by ncRNAs in orchestrating the intricate processes involved in wound healing, providing insights into potential therapeutic targets and strategies for enhancing wound healing outcomes.

Exosomes are small extracellular vesicles released by a range of cells, including mesenchymal stromal/stem cells (MSCs), immune cells, cancerous cells, etc. These particles contain biomolecules such as DNA, microRNA, messenger RNA, protein, and lipid, and play a vital role in establishing cellular communication. After reaching the target cells, the particles cause changes in function, fate, morphology, differentiation, and growth. Exosomes released from a variety of sources have the ability to influence the behavior of cells involved in wound healing, enhance neovascularization, promote collagen deposition, reduce inflammation, and quicken the healing process. According to new research, endothelial cell adhesion, migration, proliferation, vascular repair, and angiogenesis are all accelerated during the wound healing process when deleted in malignant brain tumors 1 (DMBT1) is used as an active stimulant. This article will review DMBT1 protein as one of the major elements of exosomes from human urine-derived MSCs.

Various factors can influence the complex process of wound healing. Non-coding RNAs (ncRNAs), which include long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), as well as microRNAs (miRNAs), contribute critically to the regulation of wound healing mechanisms. Specific miRNAs regulate fibroblast proliferation, migration, and extracellular matrix production, while others influence keratinocyte migration and re-epithelialization. Some miRNAs also modulate the inflammatory response and regulate angiogenesis during wound healing. The emerging significance of circRNAs in regulating fibroblast and keratinocyte functions during wound healing are also to be noted, as are the significant roles lncRNAs play in influencing various aspects of wound healing. This review underscores the pivotal roles played by ncRNAs in orchestrating the intricate processes involved in wound healing, providing insights into potential therapeutic targets and strategies for enhancing wound healing outcomes.

Exosomes are small extracellular vesicles released by a range of cells, including mesenchymal stromal/stem cells (MSCs), immune cells, cancerous cells, etc. These particles contain biomolecules such as DNA, microRNA, messenger RNA, protein, and lipid, and play a vital role in establishing cellular communication. After reaching the target cells, the particles cause changes in function, fate, morphology, differentiation, and growth. Exosomes released from a variety of sources have the ability to influence the behavior of cells involved in wound healing, enhance neovascularization, promote collagen deposition, reduce inflammation, and quicken the healing process. According to new research, endothelial cell adhesion, migration, proliferation, vascular repair, and angiogenesis are all accelerated during the wound healing process when deleted in malignant brain tumors 1 (DMBT1) is used as an active stimulant. This article will review DMBT1 protein as one of the major elements of exosomes from human urine-derived MSCs.

Various factors can influence the complex process of wound healing. Non-coding RNAs (ncRNAs), which include long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), as well as microRNAs (miRNAs), contribute critically to the regulation of wound healing mechanisms. Specific miRNAs regulate fibroblast proliferation, migration, and extracellular matrix production, while others influence keratinocyte migration and re-epithelialization. Some miRNAs also modulate the inflammatory response and regulate angiogenesis during wound healing. The emerging significance of circRNAs in regulating fibroblast and keratinocyte functions during wound healing are also to be noted, as are the significant roles lncRNAs play in influencing various aspects of wound healing. This review underscores the pivotal roles played by ncRNAs in orchestrating the intricate processes involved in wound healing, providing insights into potential therapeutic targets and strategies for enhancing wound healing outcomes.

This review explores the potential of metformin, a widely used type 2 diabetes medication, in accelerating wound healing. Derived from guanidine compounds found in Galega officinalis, a plant with a long history in traditional medicine, metformin has been recognized for its minimal side effects. Beyond its primary role in diabetes treatment, metformin shows promising non-diabetic benefits, particularly in wound healing. Research indicates that metformin enhances wound healing through multiple mechanisms. It increases circulating endothelial progenitor cells, improves vascular function, and regulates thrombospondin-1 levels. Metformin also modulates the AMPK/mTOR/NLRP3 inflammasome signaling pathway, promoting M2 macrophage polarization, which is crucial for tissue repair. Additionally, it reduces pro-inflammatory cytokines, increases growth factors, and decreases matrix metalloproteinases. Studies have shown that topical application of metformin accelerates wound contraction, closure, and overall healing. Furthermore, it has been found to reduce fibrosis-related gene expression and improve collagen synthesis. With chronic wounds affecting millions globally and causing significant healthcare costs, there is a pressing need for improved wound healing agents. This review advocates for further research to establish clinical guidelines on using metformin to enhance wound healing. By harnessing metformin’s pleiotropic effects, healthcare providers may offer personalized treatments that not only manage diabetes but also promote wound healing.

This review explores the potential of metformin, a widely used type 2 diabetes medication, in accelerating wound healing. Derived from guanidine compounds found in Galega officinalis, a plant with a long history in traditional medicine, metformin has been recognized for its minimal side effects. Beyond its primary role in diabetes treatment, metformin shows promising non-diabetic benefits, particularly in wound healing. Research indicates that metformin enhances wound healing through multiple mechanisms. It increases circulating endothelial progenitor cells, improves vascular function, and regulates thrombospondin-1 levels. Metformin also modulates the AMPK/mTOR/NLRP3 inflammasome signaling pathway, promoting M2 macrophage polarization, which is crucial for tissue repair. Additionally, it reduces pro-inflammatory cytokines, increases growth factors, and decreases matrix metalloproteinases. Studies have shown that topical application of metformin accelerates wound contraction, closure, and overall healing. Furthermore, it has been found to reduce fibrosis-related gene expression and improve collagen synthesis. With chronic wounds affecting millions globally and causing significant healthcare costs, there is a pressing need for improved wound healing agents. This review advocates for further research to establish clinical guidelines on using metformin to enhance wound healing. By harnessing metformin’s pleiotropic effects, healthcare providers may offer personalized treatments that not only manage diabetes but also promote wound healing.