**Background:** Mechanical injury—damage to anatomical structure from direct contact—is a prevalent challenge in animals, with consequences spanning molecular to ecological levels. Despite significant conservation in early wound responses across distantly related lineages, research on injury is scattered across biological subdisciplines with uneven taxonomic coverage. Biomedical research using mammalian models dominates molecular/cellular work, while organismal, ecological, and comparative studies—especially in invertebrates and non-mammalian vertebrates—are less integrated. This review aims to synthesize knowledge across biological levels and identify gaps and future directions.
**Methods:** This is a narrative review synthesizing literature on mechanical injury effects in animals across four levels of biological organization: (1) molecular and cellular effects, (2) physiological and organismal effects, (3) behavioral effects, and (4) ecological and evolutionary effects. The authors integrate findings from diverse animal groups, highlighting both conserved responses and taxonomic variation.
**Key Results:**
- Injury is pervasive: an average of roughly one-third to one-half of marine benthic invertebrate populations are visibly injured at any time; in some populations over 70% of individuals may be injured. Up to 80% of decapod crustaceans show limb damage, over 50% of lizards have tail damage, and 50–90% of anuran tadpoles have tail damage.
- At the molecular level, damage-associated molecular patterns (DAMPs), calcium signaling, and bioelectrical gradients serve as conserved early wound signals. Antimicrobial peptides (AMPs) are upregulated across cnidarians, molluscs, annelids, nematodes, arthropods, and vertebrates.
- Transcriptomic responses: injury induces differential expression of up to 9% of the transcriptome in ant queens, up to 21% in two-spotted crickets, and up to 15% in sea cucumbers. Over a thousand genes are differentially expressed in sponges, hundreds to thousands in fish.
- Metabolic rate increases following injury in annelids, planarians, insects, and brittlestars, though timing varies from hours to weeks. Growth reductions following injury are documented in corals, clams, annelids, and reptiles. Reproductive output commonly decreases but can increase in some species (e.g., pea aphids accelerate reproductive rate; anoles increase egg and hatchling size).
- Locomotory impairment from appendage loss is documented in crabs, lizards, fish, tadpoles, spiders, and others. Injury increases predation susceptibility in tadpoles, damselflies, and crabs.
- Sublethal predation can constitute major trophic input: juvenile stone flounder meet the majority of nutritional needs by cropping clam siphons; up to 70% of plaice diet in tidal flats consists of siphon tips. One bivalve species may regenerate siphons an average of 26 times in a single season.
**Clinical Implications:** While primarily a basic science review, the findings have translational relevance. Understanding why some animals heal without scarring (e.g., axolotls, spiny mice) while others scar could inform wound healing and fibrosis research in humans. The review notes that inflammation, while critical for healing in many species, may directly contribute to fibrosis and scarring—mice studies suggest some inhibition of inflammation may benefit wound repair. Spiny mice (Acomys spp.) exhibit scar-free healing and regeneration to an extent not found in other mammals, offering a model for studying regenerative medicine. The paper emphasizes that most injury research uses mammalian models, limiting generalizability, and calls for broader taxonomic sampling to uncover novel mechanisms.