The cornea is a dynamic tissue that constantly interacts with mechanical forces to maintain its structure, barrier function, transparency, and refractive power. Corneal cells sense and respond to these forces, which regulate their morphology and fate during development, homeostasis, and disease. These cells dynamically regulate their extracellular matrix (ECM), which serves as a signaling reservoir for biophysical and biochemical cues. This review provides an overview of mechanotransduction pathways and recent advances in corneal mechanobiology, focusing on the interplay between mechanical forces and responses of corneal epithelial, stromal, and endothelial cells. Species-specific differences in corneal biomechanics are identified to facilitate the selection of optimal animal models for studying corneal wound healing, disease, and therapeutic interventions. Key knowledge gaps and therapeutic opportunities in corneal mechanobiology are highlighted, particularly in the context of limbal stem cell deficiency, keratoconus, and Fuchs' endothelial corneal dystrophy. Understanding corneal mechanobiology can help contextualize discoveries related to corneal diseases and innovative treatments. The cornea experiences a wide range of mechanical forces from both external and internal sources. Externally, forces from blinking, eye rubbing, contact lenses, trauma, and infection act on the cornea. Internally, intraocular pressure generated by the balanced production and egress of aqueous humor applies a shear force on the posterior surface of the corneal endothelium. The cornea's primary cell types—epithelial, stromal, and endothelial cells—respond to different mechanical cues through mechanotransduction, altering their morphology, migration, adhesion, proliferation, differentiation, gene and protein expression, matrix production, and responsiveness to cytoactive factors. The ECM mediates receptor-ligand interactions and plays a critical role in regulating mechanical and cellular homeostasis. Mechanotransduction is the process by which the environment of a cell or tissue affects intracellular processes. It involves cellular biochemical signaling in response to extracellular, non-chemical, biophysical stimuli, including changes in topography, compliance, shear, compression, extension, gravity, and movement. Understanding mechanotransduction is crucial for studying mechanobiology, which examines how physical forces affect cellular behavior. Recent research has identified the importance of mechanotransduction in corneal diseases, including FECD, keratoconus, and Fuchs' dystrophy. Mechanotransduction occurs through various signaling pathways, including Hippo, YAP/TAZ, TGFβ, AKT, Wnt, RhoA, and Piezo1. These pathways regulate processes such as proliferation, differentiation, cytoskeletal contractility, ECM deposition, and apoptosis. The Hippo pathway is highly conserved and plays a critical role in cell proliferation, apoptosis, and stem cell regeneration. YAP/TAZ proteins areThe cornea is a dynamic tissue that constantly interacts with mechanical forces to maintain its structure, barrier function, transparency, and refractive power. Corneal cells sense and respond to these forces, which regulate their morphology and fate during development, homeostasis, and disease. These cells dynamically regulate their extracellular matrix (ECM), which serves as a signaling reservoir for biophysical and biochemical cues. This review provides an overview of mechanotransduction pathways and recent advances in corneal mechanobiology, focusing on the interplay between mechanical forces and responses of corneal epithelial, stromal, and endothelial cells. Species-specific differences in corneal biomechanics are identified to facilitate the selection of optimal animal models for studying corneal wound healing, disease, and therapeutic interventions. Key knowledge gaps and therapeutic opportunities in corneal mechanobiology are highlighted, particularly in the context of limbal stem cell deficiency, keratoconus, and Fuchs' endothelial corneal dystrophy. Understanding corneal mechanobiology can help contextualize discoveries related to corneal diseases and innovative treatments. The cornea experiences a wide range of mechanical forces from both external and internal sources. Externally, forces from blinking, eye rubbing, contact lenses, trauma, and infection act on the cornea. Internally, intraocular pressure generated by the balanced production and egress of aqueous humor applies a shear force on the posterior surface of the corneal endothelium. The cornea's primary cell types—epithelial, stromal, and endothelial cells—respond to different mechanical cues through mechanotransduction, altering their morphology, migration, adhesion, proliferation, differentiation, gene and protein expression, matrix production, and responsiveness to cytoactive factors. The ECM mediates receptor-ligand interactions and plays a critical role in regulating mechanical and cellular homeostasis. Mechanotransduction is the process by which the environment of a cell or tissue affects intracellular processes. It involves cellular biochemical signaling in response to extracellular, non-chemical, biophysical stimuli, including changes in topography, compliance, shear, compression, extension, gravity, and movement. Understanding mechanotransduction is crucial for studying mechanobiology, which examines how physical forces affect cellular behavior. Recent research has identified the importance of mechanotransduction in corneal diseases, including FECD, keratoconus, and Fuchs' dystrophy. Mechanotransduction occurs through various signaling pathways, including Hippo, YAP/TAZ, TGFβ, AKT, Wnt, RhoA, and Piezo1. These pathways regulate processes such as proliferation, differentiation, cytoskeletal contractility, ECM deposition, and apoptosis. The Hippo pathway is highly conserved and plays a critical role in cell proliferation, apoptosis, and stem cell regeneration. YAP/TAZ proteins are