Fibrosis is strongly linked with the mechanisms of atrial fibrillation (AF), the most common arrhythmia. Direct electrotonic coupling between atrial myocytes and fibroblast has been suggested to contribute to these mechanisms. We use a 3D biophysical model of the atria to study the effects of fibrosis on atrial electrophysiology. Realistic tissue geometry, regional heterogeneity and myofiber anisotropy are integrated in the model. The model also accounts for the effects AF induced ionic remodeling, which has been shown to promote AF. The model simulations demonstrated that fibrosis significantly reduced both the atrial conduction velocity and action potential duration. Both these factors contributed to a large (45%) reduction of the atrial activation wavelength. This is comparable with the wavelength reduction (65%) due to ionic remodeling. As a result, the sustenance of re- entrant waves in the 3D atria was substantially increased with both fibrosis and remodeling. Hence, the elecrotonic changes induced by fibrosis can be comparable to those due to ionic remodeling, and both factors can provide substrate for re-entry in the 3D atria model.