Glaucoma is the leading cause of irreversible blindness worldwide and is characterized by the progressive degeneration of the optic nerve. Intraocular pressure (IOP), which is considered to be the main risk factor for glaucoma development, builds up in response to the resistance (resistance to what?) provided by the trabecular meshwork (TM) to aqueous humor (AH) outflow. Although the TM and its relationship to AH outflow have remained at the forefront of scientific interest, researchers remain uncertain regarding which mechanisms drive the deterioration of the TM. Current tissue‐engineering fabrication techniques have come up with promising approaches to successfully recreate the TM. Nonetheless, more accurate models are needed to understand the factors that make glaucoma arise. In this review, we provide a chronological evaluation of the technological milestones that have taken place in the field of glaucoma research, and we conduct a comprehensive comparison of available TM fabrication technologies. Additionally, we also discuss AH perfusion platforms, since they are essential for the validation of these scaffolds, as well as pressure–outflow relationship studies and the discovery of new IOP‐reduction therapies.

Aged muscles accumulate satellite cells with a striking decline response to damage. Although intrinsic defects in satellite cells themselves are the major contributors to aging-associated stem cell dysfunction, increasing evidence suggests that changes in the muscle-stem cell local microenvironment also contribute to aging. Here, we demonstrate that loss of the matrix metalloproteinase-10 (MMP-10) in young mice alters the composition of the muscle extracellular matrix (ECM), and specifically disrupts the extracellular matrix of the satellite cell niche. This situation causes premature features of aging in the satellite cells, contributing to their functional decline and a predisposition to enter senescence under proliferative pressure. Similarly, reduction of MMP-10 levels in young satellite cells from wild type animals induces a senescence response, while addition of the protease delays this program. Significantly, the effect of MMP-10 on satellite cell aging can be extended to another context of muscle wasting, muscular dystrophy. Systemic treatment of mdx dystrophic mice with MMP-10 prevents the muscle deterioration phenotype and reduces cellular damage in the satellite cells, which are normally under replicative pressure. Most importantly, MMP-10 conserves its protective effect in the satellite cell-derived myoblasts isolated from a Duchenne muscular dystrophy patient by decreasing the accumulation of damaged DNA. Hence, MMP-10 provides a previously unrecognized therapeutic opportunity to delay satellite cell aging and overcome satellite cell dysfunction in dystrophic muscles.

Glaucoma is the second leading cause of irreversible blindness in the world according to the World Health Organization. It is characterized by the progressive degeneration of the optic nerve and despite the significant advances in the field, a cure for glaucoma remains to be found. The trabecular meshwork (TM) has been identified as the key tissue that drives pressure regulation in eye. In this review, we look over the main role of the aforementioned meshwork, as well as its outflow physiology and pathology. Research in the field of glaucoma has mostly progressed by employing animal models. However, these models are often expensive, cumbersome and exhibit a high intra-species variability. The lack of 3D in vitro models complicates the study of TM pressure regulation mechanisms, which makes it difficult to make progress in glaucoma research. In this paper, we review the time evolution of glaucoma models and discuss the ways in which tissue engineering fabrication techniques can be applied to create an artificial TM that serves as a 3D in vitro model. We also study possible outflow evaluation systems that are valid for both scaffold testing and drug screening, which may improve the understanding of TM biology.