Polycystic ovary syndrome (PCOS) is a prevalent hormonal disorder of premenopausal women worldwide and is characterized by reproductive, endocrine, and metabolic abnormalities. The clinical manifestations of PCOS include oligomenorrhea or amenorrhea, hyperandrogenism, ovarian polycystic changes, and infertility. Women with PCOS are at an increased risk of suffering from type 2 diabetes; me\tabolic syndrome; cardiovascular events, such as hypertension, dyslipidemia; gynecological diseases, including infertility, endometrial dysplasia, endometrial cancer, and ovarian malignant tumors; pregnancy complications, such as premature birth, low birthweight, and eclampsia; and emotional and mental disorders in the future. Although numerous studies have focused on PCOS, the underlying pathophysiological mechanisms of this disease remain unclear. Mitochondria play a key role in energy production, and mitochondrial dysfunction at the cellular level can affect systemic metabolic balance. The recent wide acceptance of functional mitochondrial disorders as a correlated factor of numerous diseases has led to the presupposition that abnormal mitochondrial metabolic markers are associated with PCOS. Studies conducted in the past few years have confirmed that increased oxidative stress is associated with the progression and related complications of PCOS and have proven the relationship between other mitochondrial dysfunctions and PCOS. Thus, this review aims to summarize and discuss previous and recent findings concerning the relationship between mitochondrial dysfunction and PCOS.

LAT1 is a member of the system L transporter family. The main role of the LAT1 is to transport specific amino acids through cell membranes to provide nutrients to cells and participate in several metabolic pathways. It also contributes to the transport of hormones and some drugs, which are essential for the development and treatment of some diseases. In recent years, many studies have shown that LAT1 is related to cancer, obesity, diabetes, and other diseases. However, the specific mechanism underlying the influence of LAT1 on such conditions remains unclear. Through the increasing number of studies on LAT1, we have obtained a preliminary understanding on the function of LAT1 in diseases. These studies also provide a theoretical basis for finding treatments for LAT1-related diseases, such as cancer. This review summarizes the function and mechanism of LAT1 in different diseases and the treatment of LAT1-related diseases. It also provides support for the development of novel and reliable disease treatments.