## 1 Introduction  
The cornea, a transparent avascular tissue of the anterior eye, transmits incoming light while also providing the necessary anterior refractive surface, contributing to approximately two-thirds of the eye's total refractive power [1]. The cornea is traditionally anatomically segmented into five layers, progressing from the outermost epithelium, Bowman's layer, the stroma, Descemet's membrane, to the innermost endothelium; however, it is important to acknowledge that the cornea's anatomy is, in reality, more nuanced (Figure 1) [2; 3]. The corneal endothelium, a single layer of cells lining the posterior corneal surface, regulates water flow, maintains tissue hydration at approximately 70%, and sustains clear vision by coordinating ionic pumps and tight junction barriers [4]. Among the key components of these tight junctions is ZO-1, a submembranous protein located along the apical side of the cells that contributes to structural integrity by forming hexagonal shapes and aiding in signal transduction [5; 6; 7]. While the epithelium is characterised by self-renewal and hosts a resident stem cell population in the Palisades of Vogt, human corneal endothelial cells (HCECs) typically maintain a quiescent state and demonstrate negligible in vivo proliferation [8]. By the 6 th week of human gestation, most HCECs are arrested in the G1 phase of the cell due to the suppressive effects of TGF-\(\beta\)2 present in the aqueous humour, inhibiting their entry into the S-phase [9; 10]. On average, the adult healthy human endothelium is approximately 4 \(\upmu\)m in thickness and has a cell density of 3000 cells/mm\({}^{2}\), with a gradual 0.5-0.6% decrease in central endothelial cell density annually [11; 12; 13]. Although HCECs can repair minor damage or aging-related issues by elongating and migrating, their limited in vivo proliferation capability suggests that complete repair of the endothelium following larger trauma may be unattainable [14; 15]. Factors like trauma or genetic endothelialopathies can further accelerate the decline of endothelial cell density [16; 17]. In Fuchs' dystrophy, the most common primary corneal disease, excessive abnormal Descemet's membrane secretion by enlarged endothelial cells leads to cornea guttata, impaired pump function, and corneal oedema [18]. Conditions like posterior polymorphous dystrophy, congenital hereditary endothelial dystrophy, and iridocomeal endothelial syndrome exhibit endothelial cells with epithelial-like characteristics, causing congenital corneal cloudiness and forming membranes that affect the iris and anterior chamber angle [19; 20; 21]. Additionally, damage from contact lens wear or surgical procedures can lead to endothelial cell loss, increased polymegethism and pleomorphism, and decreased transparency [22; 23; 24]. Currently, treatments for moderate corneal endothelial dysfunction and failure include transplantation of donor allo-endothelium (Table 1). Endothelial keratoplasty (EK) is a surgical procedure designed to address corneal endothelial diseases by selectively transplanting the Descemet membrane and endothelium from a donor cornea to the recipient's eye [25]. This approach aims to restore corneal clarity and enhance visual acuity by replacing dysfunctional endothelial cells, crucial for maintaining corneal deturgescence [26]. Selective endothelial replacement, initially introduced clinically by [PERSON] in 1998, presented a notably more challenging procedure compared to the traditional standard of penetrating keratoplasty (PK), which entails the complete replacement of the corneal thickness [27]. Modern techniques, such as [PERSON]'s stripping endothelial keratoplasty (DSEK) and Descemet membrane endothelial keratoplasty (DMEK), were introduced in the early 2000s [28]. These methods vary in the thickness of the transplanted tissue and surgical approach, refining the approach and offering faster visual recovery compared to traditional penetrating keratoplasty [29; 30; 31]. Figure 1: Cornea anatomy.