Background: Vascular injury in skin tissue represents a significant clinical challenge in aesthetic and regenerative medicine and is often manifested as ischemia-induced necrosis of human dermal fibroblasts (HDF). This condition is characterized by cell and tissue death resulting from impaired perfusion and may occur as a complication of dermal filler injections, trauma, or other pathological conditions. To accurately elucidate the underlying pathophysiological mechanisms and to evaluate regenerative therapeutic strategies, an in vitro model capable of replicating ischemia-induced necrosis is required. Purpose: To review the literature related to the ischemia-induced fibroblast necrosis model as a crucial foundation for understanding and addressing vascular injury in skin tissue. Method: Literature searches were conducted using PubMed, Scopus, Web of Science, and Google Scholar with relevant keywords. Results: Indicate that HDF necrosis is commonly induced by exposure to hydrogen peroxide (H₂O₂), cobalt chloride (CoCl₂), and hypoxic culture conditions to simulate oxidative stress and ischemia. Model validation is typically performed using cell viability assays (MTT), lactate dehydrogenase (LDH) release, and morphological analysis. Conclusion: Integrating hypoxia, nutrient deprivation, and oxidative stress in in vitro models offers a solid basis for studying ischemia-induced HDF necrosis and improving skin regenerative therapies, with standardized protocols boosting translational relevance. Keywords: Fibroblast Necrosis Model; Ischemia; Skin Tissue; Vascular Injury. Pendahuluan: Cedera vaskular pada jaringan kulit merupakan tantangan klinis penting dalam kedokteran estetik dan regeneratif, yang sering bermanifestasi sebagai nekrosis fibroblas dermal manusia (Human Dermal Fibroblasts/HDF) terinduksi iskemia. Kondisi ini ditandai oleh kematian sel dan jaringan akibat gangguan perfusi, dan dapat terjadi sebagai komplikasi injeksi dermal filler, trauma, maupun kondisi patologis lainnya. Untuk memahami mekanisme patofisiologis yang mendasari kondisi tersebut serta mengevaluasi potensi terapi regeneratif secara akurat, diperlukan model in vitro yang mampu mereplikasi kondisi nekrosis akibat iskemia. Tujuan: Untuk menelaah literatur terkait model nekrosis fibroblast terinduksi iskemia sebagai fondasi krusial untuk memahami dan mengatasi cedera vaskular pada jaringan kulit. Metode: Penelusuran literatur dilakukan menggunakan basis data PubMed, Scopus, Web of Science, dan Google Scholar dengan kata kunci yang relevan. Hasil: Induksi nekrosis HDF umumnya dilakukan melalui paparan hidrogen peroksida (H₂O₂), kobalt klorida (CoCl₂), serta kondisi lingkungan hipoksia untuk mensimulasikan stres oksidatif dan iskemia. Validasi model dilakukan menggunakan uji viabilitas sel (MTT), pelepasan laktat dehidrogenase (LDH), dan analisis morfologi sel. Simpulan: Integrasi hipoksia, deprivasi nutrisi, dan stres oksidatif dalam model in vitro memberikan dasar kuat untuk mempelajari nekrosis HDF terinduksi iskemia serta meningkatkan terapi regeneratif kulit, dengan protokol terstandarisasi yang memperkuat potensi translasi. Kata Kunci: Cedera Vascular; Iskemia; Jaringan Kulit; Model Nekrosis Fibroblast.