Despite advancements in investigation of cardiac fibrosis mechanisms, molecular and cellular regulation of this process remains insufficiently explored. In this context, examination of novel targets capable of regulating the state of cardiac fibroblasts and their profibrotic properties becomes a pivotal area of research. These processes include autophagy as an evolutionary conservative mechanism contributing to maintenance of cellular homeostasis through utilization of macromolecules and organelles via lysosomal degradation pathway. The objective was to investigate autophagy in cardiac fibroblasts at the early stages of cardiac dysfunction caused by pressure overload. Experimental studies showed that modelling of transverse aortic constriction promotes pressure overload with cardiomyocyte hypertrophy, perivascular fibrosis and interstitial accumulation of collagen. These morphological changes were accompanied by reduced autophagy activity in cardiac tissue. A detailed bioinformatic analysis of transcriptome of single cells revealed that modelling of cardiac dysfunction was not accompanied by changes in expression of genes associated with autophagy in total pool of cardiac fibroblasts and its subpopulations. Thus, fibroblasts demonstrated differences in specialized response to pressure overload of the heart compared to total myocardial cell pool. No change in expression of genes associated with autophagy is probably in favor of suppression of adaptation of cardiac tissue to new conditions of functioning. Autophagy as a diagnostic marker of cardiac fibrosis progression requires confirmation and additional studies.