{'fraction_non_alphanumeric': 0.019749835418038184, 'fraction_numerical': 0.003730524467851657, 'mean_word_length': 5.101740294511379, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Brief overview of the molecular structure of normal and aging human vitreous.

There is a lack of knowledge about the molecular structure of the human vitreous; also, the function and the aging processes of the vitreous are not sufficiently well understood. The human vitreous is a gel-like extracellular matrix, containing 98% water. The fibrous proteins are primarily Type II collagen fibrils, Type IX, and a hybrid of Types V and XI (Figure 1). There are proteoglycans, especially hyaluronic acid with its viscoelastic property, and fibronectin and laminin glycoproteins. There are integrins and some cells making the vitreous a real tissue. There are hyalocytes, fibroblasts, and occasional macrophages. The volume of water is approximately 4 mL to 6 mL in the human eye. There are inorganic salts and organic components of low molecular weight, soluble and insoluble proteins, hyaluronic acid, and Type II collagen, and 80% of the total vitreous collagen is of Type II. The hyaluronic acid is likely synthesized by the hyalocytes, which are probably active throughout life. It is debated whether Müller cells also play a role in the production of hyaluronic acid, which interacts with small charges of surrounding mobile ions. Changes in the ionic milieu of the vitreous may be of importance in pathologic conditions, because of adhesional forces. There is an interpenetrating network of hyaluronic acid and collagen fibrils bounded by electrostatic forces, which is responsible for interaction between the collagen and hyaluronic acid. The hyaluronic acid is hydrophilic and binds water between the collagen and the hyaluronic acid, which likely minimizes the light scattering in the vitreous. The soluble proteins are derived from plasma, and their concentration increases with age. There is also a high concentration of glycoproteins and approximately 0.43 mmol/kg of ascorbic acid. The ratio of vitreous to plasma is 9:1, but the purpose of this is not known. It is likely necessary for the ability to absorb ultraviolet light. Importantly, the vitreous is a scavenger of free radicals. The structure of the human vitreous has distinct areas with different properties and a different molecular structure. The highest density of collagen fibrils is found at the vitreous base; the highest density of hyaluronic acid is found at the vitreous cortex. There are densely packed 100-nm-thick collagen fibrils, and the vitreous cortex is thinnest over the macular area. The vitreoretinal interface can be differentiated where there is adhesion of the cortical vitreous to the internal limiting membrane. This adhesion likely results from extracellular matrix molecules. At the vitreous base, there is a perpendicular insertion of collagen fibrils into the inner aspect of the retina, which is a mechanical rather than biochemical interaction. At the posterior pole, the collagen fibrils are parallel to the retinal surface. There are two components at the vitreoretinal interface: the vitreous cortex and the internal limiting membrane, or internal limiting lamina, with some occasional cells. The internal limiting lamina is the only basal lamina of the retina, and it is the basement membrane of the Müller cells, thus containing Type IV collagen. The adhesion of the vitreous cortex and the internal limiting membrane is strongest at the disk, macula, and over retinal blood vessels, and it likely results from the extracellular matrix molecules. Fibronectin has a high affinity to Type II collagen and hyaluronic acid, and laminin has a high affinity to Type IV collagen of the basement membrane. The vitreous structure changes with age at variable speeds, and the human vitreous undergoes a slowly progressive remodeling characterized by the gradual formation of collagenous condensations and liquefied spaces in the gel structure. The molecular process of aging of the vitreous is poorly understood. What is known is that the vitreous changes from a solid gel-like state to a flaccid fluid state. The liquid vitreous increases, and the liquefaction starts centrally at the age 40 years. There is dissolution of the hyaluronic acid–collagen complex and the aggregation of collagen fibrils into bundles of parallel fibrils. There is formation of advanced glycation end products and pentosidine accumulation within the collagen. All this leads to rheologic changes of the vitreous and liquefaction and weakening of the From the Department of Ophthalmology, Klinikum der Universität München, Munich, Germany. The author reports no conflicts of interest.