Ventilator-induced diaphragm dysfunction (VIDD) may appear in patients receiving mechanical ventilation in the early stage, and has become one of the most crucial factors which result in weaning failure, which increases the incidence of pulmonary infection and other systemic complications. VIDD is characterized in diaphragmatic muscle fiber atrophy and decreased contractility, which may be attributed to reduced discharge of the phrenic nerve, increased intracellular calcium ion concentrations, and cytokine imbalance. The possible underlying mechanism may involve multiple signaling pathways, where the complex protein hydrolysis regulatory networks are activated to accelerate muscle fiber catabolism and mediate cell autophagy or apoptosis. Currently, diaphragm function can be evaluated on the basis of diaphragm excursion and thickening values through bedside ultrasonography, so as to facilitate VIDD diagnosis. Currently, there are no approaches to effectively prevent, control and relieve VIDD, such as reducing ventilator supports as soon as possible, performing combined treatment, inspiratory muscle training, phrenic nerve pacing or stimulating and nerve grafts.