Snake venom-induced tissue damage as a paradigm of redox imbalance, ferroptosis, and inflammaging.

Snakebite envenomation remains a major cause of illness globally, resulting in complex local and systemic toxic effects. Although the biochemical functions of individual snake venom components have been extensively studied, the cellular mechanisms underlying progressive tissue damage and organ dysfunction remain less well understood. This review compiles contemporary mechanistic evidence associating notable venom toxin families, such as phospholipase A₂, snake venom metalloproteinases, and three-finger toxins, with oxidative stress-induced cellular damage. Mounting evidence highlights mitochondrial dysfunction, iron release, and lipid peroxidation as central drivers of redox imbalance. New evidence supporting the idea that ferroptotic cell death plays a role in venom-induced disease is compared to more traditional types of cell death. This shows how iron-dependent oxidative injury can lead to long-term tissue damage. The review also examines how oxidative mechanisms interact with innate immune activation, endothelial dysfunction, and microvascular injury to cause organ-specific toxicity, particularly in the liver, kidneys, heart, and nervous system. This overview does not suggest a singular, unifying pathogenic pathway; instead, it emphasises representative mechanistic vignettes that influence the progression and severity of snake venom-related injury. A deeper understanding of the interactions among these pathways may enhance future research and facilitate the development of innovative strategies to improve the effectiveness of traditional antivenom therapy.