Targeting Cellular Microenvironment in Aging and Disease

Dear Colleagues,

The cellular microenvironment governs tissue development and homeostasis through multiple regulatory mechanisms, including soluble ligand–receptor interactions, extracellular vesicle release, and cell–cell- and cell–matrix-mediated intercellular communication. In addition, the physicochemical properties of the microenvironment, such as the local stiffness, viscosity, osmolarity and diffusion properties, can critically affect cellular physiology.

The cellular microenvironment changes during aging and disease. During the progression of joint diseases, such as osteoarthritis, inflammation drives the active remodeling of the extracellular matrix (ECM). ECM alterations, in turn, change the biomechanical environment of cells, which leads to metabolic changes and further drives the pathologic cascades. In cancer, ECM remodeling promotes immune escape, tumor survival and metastasis. In the brain, alterations in ECM composition and integrity contribute to the pathophysiology of epilepsy, dementia and psychiatric disorders. In neurological conditions such as stroke, multiple sclerosis and neurodegenerative diseases, EVs and the ECM regulate neuroplasticity.

In this Special Issue, we aim to explore how the cellular microenvironment can be targeted to prevent or modify the time course of diseases in different organs, including the brain, cartilage, skin, liver, lung, kidney and cardiovascular system. Particularly, but not exclusively, we expect to collect reviews, as well as experimental and bioinformatic studies focusing on the following:

• New mechanisms of extracellular signaling, particularly “vicious cycles” linking impaired proteostasis, aggregation of peptides/proteins, extracellular vesicle release and inflammation with ECM and tissue remodeling;
• Cellular dysfunctions during acute and chronic phases of tissue repair triggered by the dysregulation of extracellular proteases and their tissue inhibitors;
• Role of extracellular vesicles in pathophysiological and recovery mechanisms;
• Novel antifibrotic strategies;
• Drugs targeting biosynthesis, glycosylation, proteolysis and other posttranslational modifications of ECM molecules and their receptors, and related biomarkers;
• Emerging gene therapies targeting the regulation of ECM abundance and composition.

Prof. Dr. Alexander Dityatev
Dr. Egor Dzyubenko
Guest Editors

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• proteoglycans
• glycans
• glycoproteins
• matricellular proteins
• integrins
• matrix metalloproteinases
• extracellular vesicles
• EV release
• exosomes
• extracellular scaffold
• ECM remodeling
• fibrosis
• ECM gene therapy
• ECM pharmacology
• synthetic ECM