Characterization of varicocele-induced animal models: Potential role of inflammasome complex in the varicocele pathophysiology

Varicocele mechanisms and its impact in testicular dysfunction has been studied in order to understand the pathophysiology involved in this disease. However, study designs using testicular tissues from varicocele patients are restricted due to ethical limitations. Therefore, the use of animal models, mainly rats, that mimics varicocele and its effects is an option to develop new approaches. The surgical technique, that induces the varicocele in rats, is based on the partial obstruction of the left renal vein, leading to a dilation in the left spermatic vein and consequently to the pampiniform plexus, resulting in varicocele-induced condition. Thus, the study of the cellular and molecular mechanisms involved in varicocele development can be addressed in depth. Besides the animal model goal to uncover the exact varicocele pathophysiology, varicocele induced models are the best options to develop new non-surgical and less invasive therapies. Various animal model studies designed and investigated antioxidant and anti-inflammatory agents to face varicocele conditions. Minding this fact, we tried to discuss a newly uncovered complex in varicocele condition, known as inflammasome complex. Taking into consideration the possible inflammatory state present in varicocele, the inflammasome complex has been proposed to be involved in the pathophysiology of this disease.

Automated summary

Research on varicocele mechanisms using animal models, particularly rats, is crucial due to ethical restrictions on human tissue study designs. Inducing varicocele in rats through surgical techniques provides insights into the pathophysiology, allowing for the development of new therapeutic approaches. Animal models also aid in exploring antioxidant and anti-inflammatory agents to address varicocele conditions, with a focus on the newly uncovered inflammasome complex's potential role in the disease's pathophysiology.