Dry eye syndrome, also known as dry eye disease (DED), affects approximately 10–30% of the population in China[1]. It is characterized by reduced tear production, abnormalities in tear film stability, excessive tear evaporation, or an imbalance in tear composition[2, 3]. Individuals with DED often experience symptoms such as dryness, redness, pain, blurred vision, light sensitivity, and a burning sensation[4]. Severe DED can lead to corneal damage, including ulcers, erosions, or even permanent scarring[5]. Moreover, the persistent discomfort and pain can be emotionally distressing, significantly reducing quality of life and affecting daily activities[6].
In clinical practice, common therapeutic approaches include prescribed medications like artificial tears and anti-inflammatory eye drops; lifestyle modifications such as wearing moisture chamber spectacles and engaging in specific exercises; and physiotherapy techniques like meibomian gland massage and acupuncture[7–9]. Although current treatments primarily focus on symptomatic relief, a substantial number of patients with complex medical conditions or pathogenic factors rarely achieve significant efficacy[10]. Therefore, investigating the mechanisms of this disease may lead to more effective treatment options for DED.
Several biochemical mechanisms contribute to the development of DED. Chronic inflammation, widely confirmed to affect tear secretion, stability, and quality, triggers immune system abnormalities and infections[11]. Additionally, abnormal ocular surface structures, such as meibomian gland dysfunction, may increase tear evaporation[12]. Furthermore, alterations in certain chemical components within the body, such as hormonal fluctuations, particularly in females, medication side effects, and nutritional deficiencies, are also associated with DED[13–14]. These factors often interact, exacerbating DED.
Recent studies report that oxidative stress plays a significant role in the development and progression of dry eye disease (DED)[15]. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and antioxidants[16]. In DED, this imbalance leads to increased production of ROS such as superoxide radicals and hydrogen peroxide, resulting in damage to the cornea, conjunctiva, and meibomian gland[17]. Furthermore, ROS can induce cellular dysfunction and injury by oxidizing lipids, proteins, and DNA, thereby triggering inflammatory responses that exacerbate the disruption of the ocular microenvironment[18–19]. Additionally, oxidative stress can activate the ocular immune system, amplifying inflammation in DED[19].
Poly (rC) binding protein 1 (PCBP-1), a prominent member of the PCBP protein family, is expressed in various human tissues. Initially identified as part of the heterogeneous nuclear ribonucleoprotein complex hnRNP E1, PCBP1 influences various cellular processes, including mRNA stability, translation, and transcription, which affect gene expression[20]. The loss of PCBP1 is linked to cell cycle delays, DNA damage, and reduced viability[21]. PCBP1 also acts as an iron molecular chaperone, controlling the chemical reactions in cells related to iron perception and transport[22,23].
Ferroptosis, a type of cell death discovered relatively recently, differs from traditional forms like apoptosis and necrosis[24]. It is characterized by iron-dependent lipid peroxide accumulation within cells[25]. Recent research indicates that ferroptosis may play a role in DED. One study revealed that cells from the lacrimal glands of DED patients were more susceptible to ferroptosis compared to those from healthy individuals[26]. Another study demonstrated that inhibiting ferroptosis reduced DED symptoms in an animal model[27]. Notably, oxidative stress is a primary driver of ferroptosis, particularly due to lipid peroxidation and iron's role in ROS formation via the Fenton reaction[28].
Given the unknown specific mechanisms by which ferroptosis and oxidative stress influence DED, thorough investigations are crucial. Therefore, this paper seeks to identify a key protein via bioinformatics analysis and further explore its involvement in DED through ferroptosis or oxidative stress in a DED model. protein was involved in DED via ferroptosis or oxidative stress in DED model.