Biochemical Pathways of Cellular Mechanosensing/Mechanotransduction and Their Role in Neurodegenerative Diseases Pathogenesis

In this review, we shed light on recent advances regarding the characterization of biochemical pathways of cellular mechanosensing and mechanotransduction with particular attention to their role in neurodegenerative disease pathogenesis. While the mechanistic components of these pathways are mostly...

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Main Authors: Ilaria Tortorella, Chiara Argentati, Carla Emiliani, Francesco Morena, Sabata Martino
Format: Article
Language:English
Published: MDPI AG 2022-10-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/11/19/3093
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author Ilaria Tortorella
Chiara Argentati
Carla Emiliani
Francesco Morena
Sabata Martino
author_facet Ilaria Tortorella
Chiara Argentati
Carla Emiliani
Francesco Morena
Sabata Martino
author_sort Ilaria Tortorella
collection DOAJ
description In this review, we shed light on recent advances regarding the characterization of biochemical pathways of cellular mechanosensing and mechanotransduction with particular attention to their role in neurodegenerative disease pathogenesis. While the mechanistic components of these pathways are mostly uncovered today, the crosstalk between mechanical forces and soluble intracellular signaling is still not fully elucidated. Here, we recapitulate the general concepts of mechanobiology and the mechanisms that govern the mechanosensing and mechanotransduction processes, and we examine the crosstalk between mechanical stimuli and intracellular biochemical response, highlighting their effect on cellular organelles’ homeostasis and dysfunction. In particular, we discuss the current knowledge about the translation of mechanosignaling into biochemical signaling, focusing on those diseases that encompass metabolic accumulation of mutant proteins and have as primary characteristics the formation of pathological intracellular aggregates, such as Alzheimer’s Disease, Huntington’s Disease, Amyotrophic Lateral Sclerosis and Parkinson’s Disease. Overall, recent findings elucidate how mechanosensing and mechanotransduction pathways may be crucial to understand the pathogenic mechanisms underlying neurodegenerative diseases and emphasize the importance of these pathways for identifying potential therapeutic targets.
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spelling doaj.art-e3fb3e14a6f847b8ac5dd5bc3fe69dc72023-11-23T20:02:40ZengMDPI AGCells2073-44092022-10-011119309310.3390/cells11193093Biochemical Pathways of Cellular Mechanosensing/Mechanotransduction and Their Role in Neurodegenerative Diseases PathogenesisIlaria Tortorella0Chiara Argentati1Carla Emiliani2Francesco Morena3Sabata Martino4Department of Chemistry, Biology and Biotechnology, University of Perugia, Via del Giochetto, 06123 Perugia, ItalyDepartment of Chemistry, Biology and Biotechnology, University of Perugia, Via del Giochetto, 06123 Perugia, ItalyDepartment of Chemistry, Biology and Biotechnology, University of Perugia, Via del Giochetto, 06123 Perugia, ItalyDepartment of Chemistry, Biology and Biotechnology, University of Perugia, Via del Giochetto, 06123 Perugia, ItalyDepartment of Chemistry, Biology and Biotechnology, University of Perugia, Via del Giochetto, 06123 Perugia, ItalyIn this review, we shed light on recent advances regarding the characterization of biochemical pathways of cellular mechanosensing and mechanotransduction with particular attention to their role in neurodegenerative disease pathogenesis. While the mechanistic components of these pathways are mostly uncovered today, the crosstalk between mechanical forces and soluble intracellular signaling is still not fully elucidated. Here, we recapitulate the general concepts of mechanobiology and the mechanisms that govern the mechanosensing and mechanotransduction processes, and we examine the crosstalk between mechanical stimuli and intracellular biochemical response, highlighting their effect on cellular organelles’ homeostasis and dysfunction. In particular, we discuss the current knowledge about the translation of mechanosignaling into biochemical signaling, focusing on those diseases that encompass metabolic accumulation of mutant proteins and have as primary characteristics the formation of pathological intracellular aggregates, such as Alzheimer’s Disease, Huntington’s Disease, Amyotrophic Lateral Sclerosis and Parkinson’s Disease. Overall, recent findings elucidate how mechanosensing and mechanotransduction pathways may be crucial to understand the pathogenic mechanisms underlying neurodegenerative diseases and emphasize the importance of these pathways for identifying potential therapeutic targets.https://www.mdpi.com/2073-4409/11/19/3093mechanosensingmechanotransductionneurodegenerative diseasesmechanobiologyAlzheimer’s DiseaseHuntington’s Disease
spellingShingle Ilaria Tortorella
Chiara Argentati
Carla Emiliani
Francesco Morena
Sabata Martino
Biochemical Pathways of Cellular Mechanosensing/Mechanotransduction and Their Role in Neurodegenerative Diseases Pathogenesis
Cells
mechanosensing
mechanotransduction
neurodegenerative diseases
mechanobiology
Alzheimer’s Disease
Huntington’s Disease
title Biochemical Pathways of Cellular Mechanosensing/Mechanotransduction and Their Role in Neurodegenerative Diseases Pathogenesis
title_full Biochemical Pathways of Cellular Mechanosensing/Mechanotransduction and Their Role in Neurodegenerative Diseases Pathogenesis
title_fullStr Biochemical Pathways of Cellular Mechanosensing/Mechanotransduction and Their Role in Neurodegenerative Diseases Pathogenesis
title_full_unstemmed Biochemical Pathways of Cellular Mechanosensing/Mechanotransduction and Their Role in Neurodegenerative Diseases Pathogenesis
title_short Biochemical Pathways of Cellular Mechanosensing/Mechanotransduction and Their Role in Neurodegenerative Diseases Pathogenesis
title_sort biochemical pathways of cellular mechanosensing mechanotransduction and their role in neurodegenerative diseases pathogenesis
topic mechanosensing
mechanotransduction
neurodegenerative diseases
mechanobiology
Alzheimer’s Disease
Huntington’s Disease
url https://www.mdpi.com/2073-4409/11/19/3093
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