Obesity is increasingly prevalent globally and is associated with various diseases, including diabetes, coronary heart disease, and metabolic syndrome. It significantly impacts wound healing, with obese patients experiencing delayed healing due to factors such as chronic low-grade inflammation, altered immune responses, and changes in vascularity. Adipokines, cytokines, and chemokines play a key role in this process, contributing to poor wound healing outcomes. Obesity also affects the four phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. The inflammatory phase is prolonged in obese individuals, leading to delayed healing. Animal models such as the hypertrophic wound model, wound-induced hair follicle neogenesis model, and excisional wound model are used to study wound healing. These models help in understanding the effects of obesity on wound healing and in developing therapeutic strategies. Diet-induced obesity and genetic models of obesity, such as ob/ob and db/db mice, are also used to study the impact of obesity on wound healing. These models show that obesity impairs wound healing through mechanisms involving inflammation, altered immune responses, and changes in vascularity. Future research should focus on understanding the mechanisms of wound healing in obesity and developing strategies to improve healing outcomes. The use of animal models in studying obesity-related wound healing is essential for advancing our understanding and developing effective treatments. Obesity-induced chronic low-grade inflammation and increased production of pro-inflammatory adipokines, cytokines, and chemokines contribute to poor wound healing. Continued research is needed to explore these mechanisms and improve wound healing in obese populations.Obesity is increasingly prevalent globally and is associated with various diseases, including diabetes, coronary heart disease, and metabolic syndrome. It significantly impacts wound healing, with obese patients experiencing delayed healing due to factors such as chronic low-grade inflammation, altered immune responses, and changes in vascularity. Adipokines, cytokines, and chemokines play a key role in this process, contributing to poor wound healing outcomes. Obesity also affects the four phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. The inflammatory phase is prolonged in obese individuals, leading to delayed healing. Animal models such as the hypertrophic wound model, wound-induced hair follicle neogenesis model, and excisional wound model are used to study wound healing. These models help in understanding the effects of obesity on wound healing and in developing therapeutic strategies. Diet-induced obesity and genetic models of obesity, such as ob/ob and db/db mice, are also used to study the impact of obesity on wound healing. These models show that obesity impairs wound healing through mechanisms involving inflammation, altered immune responses, and changes in vascularity. Future research should focus on understanding the mechanisms of wound healing in obesity and developing strategies to improve healing outcomes. The use of animal models in studying obesity-related wound healing is essential for advancing our understanding and developing effective treatments. Obesity-induced chronic low-grade inflammation and increased production of pro-inflammatory adipokines, cytokines, and chemokines contribute to poor wound healing. Continued research is needed to explore these mechanisms and improve wound healing in obese populations.