Diabetes affects an increasing number of patients, and is associated with sustained and chronic inflammation. Complications arising from diabetes, including hypoxia, neuropathy, hyperglycemia, and ischemia that contribute to a delayed and reduced healing response result in chronic slow healing wounds. Here, key differences in native versus diabetic wound healing during each phase of healing are discussed, and the roles of cells and their secreted cytokines which regulate this process are outlined. Monocyte chemoattractant protein-1 (MCP-1) is a pro-inflammatory mediator which plays a key role in modulating angiogenesis. Its importance in diabetic wound healing as well as recent work using MCP-1 and similar chemokines to reduce inflammation and improve healing are reviewed. The delayed healing response observed in diabetic patients often results in the formation of slow healing wounds, commonly presenting in the lower extremities as diabetic foot ulcers (DFUs); classification systems and current treatment options for DFUs, including debridement, off-loading, and amputation are outlined. Common dressing strategies are highlighted, and recent work developing biocompatible and bioactive hydrogels to address and hasten chronic wound healing is focused on.