Skin tissue regeneration requires coordinated responses from immune cells, keratinocytes, fibroblasts, vascular endothelial cells, and other cell populations. Wound closure restores tissue continuity, but it does not necessarily indicate recovery of the epidermal barrier, dermal architecture, skin appendages, or tissue function. Chronic wounds and pathological scars are distinct manifestations of dysregulated repair: the former are commonly associated with persistent inflammation and impaired tissue formation, whereas the latter involve excessive extracellular matrix deposition and fibrosis. Their distinct pathological settings need to be considered when interpreting mechanisms and evaluating interventions. Network pharmacology integrates information on drug constituents, candidate targets, signaling pathways, and disease phenotypes to generate testable hypotheses about multicomponent and multitarget drug actions. It can narrow the range of candidates for subsequent studies, but associations derived from databases, network topology, functional enrichment, or molecular docking do not establish direct target engagement or a causal contribution to tissue regeneration. This review summarizes the biological basis and representative regulatory networks of skin wound repair and tissue regeneration, outlines the main steps and limitations of network pharmacology, and examines how it can be integrated with other techniques. Transcriptomics, proteomics, phosphoproteomics, and metabolomics can compare predicted networks with molecular responses measured in treated samples. Single-cell sequencing and spatial omics can further locate candidate targets in specific cell populations and wound regions, while sampling across repair stages helps assess their temporal context. Machine-learning methods can rank candidate targets for experimental follow-up, provided that model performance is evaluated using appropriate validation procedures. Biochemical and biophysical approaches, including direct binding assays and measurements of protein activity, can test whether a predicted drug-target relationship is supported at the molecular level. Target inhibition or genetic perturbation, together with rescue experiments where feasible, can then assess whether the target contributes to an observed drug response. Cell-based assays and animal studies can relate these molecular findings to processes such as re-epithelialization, angiogenesis, extracellular matrix remodeling, and restoration of skin structure. Together, these approaches can prioritize candidate targets and relate predicted drug actions to molecular, cellular, and tissue-level observations. Agreement between network predictions and experimental observations can support a proposed mechanism, but it does not, by itself, establish a causal role for the target. Database coverage and target-prediction algorithms can bias candidate selection; commonly used oral bioavailability and drug-likeness thresholds may be poorly suited to topical treatment; and the composition and tissue exposure of multicomponent preparations are not always known. In addition, target effects may vary among wound types, cell populations, anatomical regions, and repair stages. Two-dimensional cell cultures and animal models cannot fully reproduce human chronic wounds, and promising experimental results do not by themselves demonstrate clinical benefit. Together, these limitations may affect the reliability and applicability of network predictions. Future work should standardize data sources and reporting, account for pathological and spatiotemporal context, and use direct target-engagement and causal-intervention experiments to test key hypotheses. Drug dose, route of administration, local exposure, formulation stability, and safety should be evaluated alongside healing outcomes. Beyond wound area and inflammatory changes, endpoints should include barrier recovery, tissue architecture, relevant skin appendages, and functional properties when the injury model permits. A connected evidence pathway from network prediction through molecular and biological validation to clinically relevant evaluation may provide a more reliable basis for studying drugs intended to improve skin wound repair and tissue regeneration.