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Bats rely on their hand-wings to execute agile flight maneuvers, to grasp objects, and cradle young. Embedded in the dorsal and ventral membranes of bat wings are microscopic hairs. Past research findings implicate dorsal wing hairs in airflow sensing for flight control, but the function of ventral wing hairs has not been previously investigated. Here, we test the hypothesis that ventral wing hairs carry mechanosensory signals for flight control, prey capture, and handling. To test this hypothesis, we used synchronized high-speed stereo video and audio recordings to quantify flight and echolocation behaviors of big brown bats (Eptesicus fuscus) engaged in an aerial insect capture task. We analyzed prey-capture strategy and performance, along with flight kinematics, before and after depilation of microscopic hairs from the bat's ventral wing and tail membranes. We found that ventral wing hair depilation significantly impaired the bat's prey-capture performance. Interestingly, ventral wing hair depilation also produced increases in the bat's flight speed, an effect previously attributed exclusively to airflow sensing along the dorsal wing surface. These findings demonstrate that microscopic hairs embedded in the ventral wing and tail membranes of insectivorous bats provide mechanosensory feedback for prey handling and flight control. [ABSTRACT FROM AUTHOR]

Mechanical forces influence different cell types in our bodies. Among the earliest forces experienced in mammals is blood movement in the vascular system. Blood flow starts at the embryonic stage and ceases when the heart stops. Blood flow exposes endothelial cells (ECs) that line all blood vessels to hemodynamic forces. ECs detect these mechanical forces (mechanosensing) through mechanosensors, thus triggering physiological responses such as changes in vascular diameter. In this review, we focus on endothelial mechanosensing and on how different ion channels, receptors, and membrane structures detect forces and mediate intricate mechanotransduction responses. We further highlight that these responses often reflect collaborative efforts involving several mechanosensors and mechanotransducers. We close with a consideration of current knowledge regarding the dysregulation of endothelial mechanosensing during disease. Because hemodynamic disruptions are hallmarks of cardiovascular disease, studying endothelial mechanosensing holds great promise for advancing our understanding of vascular physiology and pathophysiology. [ABSTRACT FROM AUTHOR]

Disturbed flow promotes progression of atherosclerosis at particular regions of arteries where the recent studies show the arterial wall becomes stiffer. Objective of this study is to show how mechanotransduction in subcellular organelles of endothelial cells (ECs) will alter with changes in blood flow profiles applied on ECs surface and mechanical properties of arterial wall where ECs are attached to. We will examine the exposure of ECs to atherogenic flow profiles (disturbed flow) and non-atherogenic flow profiles (purely forward flow), while stiffness and viscoelasticity of arterial wall will change. A multicomponent model of endothelial cell monolayer was applied to quantify the response of subcellular organelles to the changes in their microenvironment. Our results show that arterial stiffening alters mechanotransduction in intra/inter-cellular organelles of ECs by slight increase in the transmitted stresses, particularly over central stress fibers (SFs). We also observed that degradation of glycocalyx and exposure to non-atherogenic flow profiles result in significantly higher stresses in subcellular organelles, while degradation of glycocalyx and exposure to atherogenic flow profiles result in dramatically lower stresses in the organelles. Moreover, we show that increasing the arterial wall viscoelasticity leads to slight increase in the stresses transmitted to subcellular organelles. FAs are particularly influenced with the changes in the arterial wall properties and viscoelasticity. Our study suggests that changes in viscoelasticity of arterial wall and degradation state of glycocalyx have to be considered along with arterial stiffening in designing more efficient treatment strategies for atherosclerosis. Our study provides insight into significant role of mechanotransduction in the localization of atherosclerosis by quantifying the role of ECs mechanosensors and suggests that mechanotransduction may play a key role in design of more efficient and precision therapeutics to slow down or block the progression of atherosclerosis. [ABSTRACT FROM AUTHOR]

Bio‐inspired cilium‐based mechanosensors offer a high level of responsiveness, making them suitable for a wide range of industrial, environmental, and biomedical applications. Despite great promise, the development of sensors with multifunctionality, scalability, customizability, and sensing linearity presents challenges due to the complex sensing mechanisms and fabrication methods involved. To this end, high‐aspect‐ratio polycaprolactone/graphene cilia structures with high conductivity, and facile fabrication are employed to address these challenges. For these 3D‐printed structures, an "inter‐cilium contact" sensing mechanism that enables the sensor to function akin to an on‐off switch, significantly enhancing sensitivity and reducing ambiguity in detection, is proposed. The cilia structures exhibit high levels of customizability, including thickness, height, spacing, and arrangement, while maintaining mechanical robustness. The simplicity of the sensor design enables highly sensitive detection in diverse applications, encompassing airflow and water flow monitoring, braille detection, and debris recognition. Overall, the unique conductive cilia‐based sensing mechanism that is proposed brings several advantages, advancing the development of multi‐sensing capabilities and flexible electronic skin applications in smart robotics and human prosthetics. [ABSTRACT FROM AUTHOR]

The ability of skeletal muscles to sense mechanical stimuli and respond to them by changing intracellular electrochemical and biochemical processes (mechanotransduction) is of crucial importance for the regulation of physiological processes in muscle fibers. This review describes the main sarcolemmal, sarcomeric, and cytoskeletal mechanosensitive structures and analyzes mechano-dependent signaling pathways and mechanisms involved in the regulation of gene expression, as well as muscle protein synthesis and degradation. The final part of the review formulates specific questions in the field of muscle mechanotransduction that need to be addressed in future studies. The understanding of skeletal muscle mechanotransduction is required for the development of effective measures aimed at the treatment of muscular dystrophies, sarcopenia, and prevention of disuse-induced muscle atrophy. [ABSTRACT FROM AUTHOR]

Abstract Bio‐inspired cilium‐based mechanosensors offer a high level of responsiveness, making them suitable for a wide range of industrial, environmental, and biomedical applications. Despite great promise, the development of sensors with multifunctionality, scalability, customizability, and sensing linearity presents challenges due to the complex sensing mechanisms and fabrication methods involved. To this end, high‐aspect‐ratio polycaprolactone/graphene cilia structures with high conductivity, and facile fabrication are employed to address these challenges. For these 3D‐printed structures, an “inter‐cilium contact” sensing mechanism that enables the sensor to function akin to an on‐off switch, significantly enhancing sensitivity and reducing ambiguity in detection, is proposed. The cilia structures exhibit high levels of customizability, including thickness, height, spacing, and arrangement, while maintaining mechanical robustness. The simplicity of the sensor design enables highly sensitive detection in diverse applications, encompassing airflow and water flow monitoring, braille detection, and debris recognition. Overall, the unique conductive cilia‐based sensing mechanism that is proposed brings several advantages, advancing the development of multi‐sensing capabilities and flexible electronic skin applications in smart robotics and human prosthetics.

Hui Li,* Wen-Ying Zhou,* Yi-Yuan Xia,* Jun-Xia Zhang Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210006, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jun-Xia Zhang, Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210006, People’s Republic of China, Tel +86 15366155682, Email zhangjunshia@njmu.edu.cnAbstract: Vascular endothelial cells (ECs), derived from the mesoderm, form a single layer of squamous cells that covers the inner surface of blood vessels. In addition to being regulated by chemical signals from the extracellular matrix (ECM) and blood, ECs are directly confronted to complex hemodynamic environment. These physical inputs are translated into biochemical signals, dictating multiple aspects of cell behaviour and destination, including growth, differentiation, migration, adhesion, death and survival. Mechanosensors are initial responders to changes in mechanical environments, and the overwhelming majority of them are located on the plasma membrane. Physical forces affect plasma membrane fluidity and change of protein complexes on plasma membrane, accompanied by altering intercellular connections, cell-ECM adhesion, deformation of the cytoskeleton, and consequently, transcriptional responses in shaping specific phenotypes. Among the diverse forces exerted on ECs, shear stress (SS), defined as tangential friction force exerted by blood flow, has been extensively studied, from mechanosensing to mechanotransduction, as well as corresponding phenotypes. However, the precise mechanosensors and signalling pathways that determine atheroprone and atheroprotective phenotypes of arteries remain unclear. Moreover, it is worth to mention that some established mechanosensors of atheroprotective SS, endothelial glycocalyx, for example, might be dismantled by atheroprone SS. Therefore, we provide an overview of the current knowledge on mechanosensors in ECs for SS signals. We emphasize how these ECs coordinate or differentially participate in phenotype regulation induced by atheroprone and atheroprotective SS.Keywords: shear stress, endothelial cells, mechanosensors, mechanotransduction

Mechanobiology is a domain of interdisciplinary research that aims to explore the impact of physical force, applied externally or internally, on cell and tissue function, including development, growth, and differentiation. Mechanotransduction is a term that describes how cells sense physical forces (such as compression, stretch, and shear stress), convert them into biochemical signals, and mount adaptive responses integrated by the nucleus. There is accumulating evidence that mechanical forces extensively inform the biological behaviour of liver cells in health and disease. Recent research has elucidated many cellular and molecular mechanisms involved in this process including the pleiotropic control and diverse effects of the paralogous transcription co-activators YAP/TAZ, which play a prominent role in mechanotransduction. The liver sinusoids represent a unique microenvironment in which cells are exposed to mechanical cues originating in the cytoskeleton and at interfaces with adjacent cells, the extracellular matrix, and vascular or interstitial fluids. In non-alcoholic fatty liver disease (NAFLD), hepatocellular lipid accumulation and ballooning, activation of inflammatory responses, dysfunction of liver sinusoidal endothelial cells, and transdifferentiation of hepatic stellate cells into a pro-contractile and pro-fibrotic phenotype have been associated with aberrant cycles of mechanosensing and mechanoresponses. The downstream consequences of disrupted mechanical homeostasis likely contribute to the progression of NAFLD and promote the development of portal hypertension, cirrhosis, and hepatocellular carcinoma. Identification of molecular targets involved in pathogenic mechanotransduction will allow for the development of novel strategies to prevent the progression of liver disease in NAFLD. [ABSTRACT FROM AUTHOR]

Internal mechanosensors, as the core component of a proprioceptive system, provide vital mechanical information from intelligent devices for adaptive motor control, mechanical fault diagnosis, and machining condition monitoring. However, developing a sophisticated mechanosensory structure that can be widely used is highly desirable to significantly improve the detection performance of internal mechanosensors. Coincidentally, in nature, optimized microscale slits of arachnids (e.g., scorpions and spiders) are ingeniously used as a mechanosensory structure for internal mechanosensilla to efficiently detect the inevitable internal mechanical feedbacks caused by self‐motion and external mechanical stimuli. Biological slit‐based mechano‐sensilla provide an attractive bio‐inspired strategy to use the controllable slit as the sensory structure to improve the perceptual performance of internal mechanosensors. In this study, the structure‐deformation‐performance coupling relationship of slit‐based mechano‐sensilla is explored through experiment and theoretical analysis. An artificial slit‐based mechanosensor is developed by mimicking the combined deformation properties of the slit and the ultrathin cuticular membrane covering the slit tail. This bio‐inspired mechanosensor shows excellent performance in terms of mechanical stability, response time, and sensitivity to mechanical signals. The research on a practical application highlights the importance of the unique basic "design" principles of the slit‐based mechano‐sensilla in improving the proprioceptive capability of smart engineering devices. [ABSTRACT FROM AUTHOR]

Background Lipoprotein lipase (LPL)‐derived fatty acid is a major source of energy for cardiac contraction. Synthesized in cardiomyocytes, LPL requires translocation to the vascular lumen for hydrolysis of lipoprotein triglyceride, an action mediated by endothelial cell (EC) release of heparanase. We determined whether flow‐mediated biophysical forces can cause ECs to secrete heparanase and thus regulate cardiac metabolism. Methods and Results Isolated hearts were retrogradely perfused. Confluent rat aortic ECs were exposed to laminar flow using an orbital shaker. Cathepsin L activity was determined using gelatin‐zymography. Diabetes was induced in rats with streptozotocin. Despite the abundance of enzymatically active heparanase in the heart, it was the enzymatically inactive, latent heparanase that was exceptionally responsive to flow‐induced release. EC exposed to orbital rotation exhibited a similar pattern of heparanase secretion, an effect that was reproduced by activation of the mechanosensor, Piezo1. The laminar flow‐mediated release of heparanase from EC required activation of both the purinergic receptor and protein kinase D, a kinase that assists in vesicular transport of proteins. Heparanase influenced cardiac metabolism by increasing cardiomyocyte LPL displacement along with subsequent replenishment. The flow‐induced heparanase secretion was augmented following diabetes and could explain the increased heparin‐releasable pool of LPL at the coronary lumen in these diabetic hearts. Conclusions ECs sense fluid shear‐stress and communicate this information to subjacent cardiomyocytes with the help of heparanase. This flow‐induced mechanosensing and its dynamic control of cardiac metabolism to generate ATP, using LPL‐derived fatty acid, is exquisitely adapted to respond to disease conditions, like diabetes.

Introduction—Local hemodynamics impact the mechanotransduction in endothelial cells (ECs) lining the vascular network. On the other hand, cancer cells are shown to influence the local hemodynamics in their vicinity, in microvasculature. The first objective of present study is to explore how cancer cell-induced changes in local hemodynamics can impact the forces experienced by intra/inter-cellular organelles of ECs that are believed to play important roles in mechanotransduction. Moreover, extracellular matrix (ECM) stiffening has been shown to correlate with progression of most cancer types. However, it is still not well understood how ECM stiffness impacts ECs mechanosensors. The second objective of this study is to elucidate the role of ECM stiffness on mechanotransduction in ECs. Methods—A three-dimensional, multiscale, multicomponent, viscoelastic model of focally adhered ECs is developed to simulate the force transmission through ECs mechanosensors [actin cortical layer, nucleus, cytoskeleton, focal adhesions (FAs), and adherens junctions (ADJs)]. Results—Our results show that cancer cell-altered hemodynamics results in significantly high forces transmitted to subcellular organelles of ECs which are in vicinity of cancer cells. This impact is more drastic on stress fibers (SFs) both centrally located and peripheral ones. Furthermore, we demonstrate that ADJs, FAs, and SFs experience higher stresses in ECs attached to stiffer ECM. Impact of ECM stiffness is particularly significant in ECs exposed to fluid shear stresses of 2 Pa or lower. This finding reveals the role of organ-specific stiffness in promoting cancer cell transmigration even in capillaries larger than cancer cell diameter. Conclusions—ÊCancer cell-induced-changes in ECs mechanotransduction represents an important potential mechanism for cancer cell transmigration in the microvasculature particularly with stiffer ECM. The identification of ECs mechanosensors involved in early stages of EC-cancer cell interaction will help with developing more efficient therapeutic interventions to suppress cancer cell transmigration in the microvasculature. [ABSTRACT FROM AUTHOR]

In an effort to develop the next generation of neural implants, current research has focused on solving the challenges associated with the foreign body reaction and promoting long‐term device performance in vivo. Although the cutting edge of research in this field appears to be moving away from traditional metallic and semiconductor materials, the complex tissue dynamics which occur at the electrode–neural interface following device implantation are yet to be resolved. In particular, understanding the molecular processes of gliosis and the onset and persistence of scar formation is key in developing stable and specific neural recording/stimulation devices. Critically, it is recognized that neural device implantation leads to a significant disruption of tissue integrity at the peri‐electrode site. Accordingly, an in‐depth understanding of mechanotransduction in neuronal cell populations at the peri‐implant region is required to better inform neural interface design. This perspective highlights the need for a comprehensive mechanobiological understanding of gliosis to enhance the development of neural implants with improved chronic functionality.

Hepatocellular carcinoma (HCC) is the sixth most common cancer in the world and the third leading cause of cancer deaths globally. More than 80% of HCC patients have a background of fibrosis or cirrhosis, which leads to changes in physical factors in tumor microenvironment (TME), such as increased stiffness, solid stress, fluid stresses and structural alterations in the extracellular matrix (ECM). In the past, the focus of cancer research has predominantly been on genetic and biochemical factors in the TME, and the critical role of physical factors has often been overlooked. Recent discoveries suggest these unique physical signals are converted into biochemical signals through a mechanotransduction process that influences the biological behavior of tumor cells and stromal cells. This process facilitates the occurrence and progression of tumors. This review delves into the alterations in the mechanical microenvironment during the progression of liver fibrosis to HCC, the signaling pathways activated by physical signals, and the effects on both tumor and mesenchymal stromal cells. Furthermore, this paper summarizes and discusses the therapeutic options for targeting the mechanical aspects of the TME, offering valuable insights for future research into novel therapeutic avenues against HCC and other solid tumors., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Two conventional doctrines govern airway mechanosensory interpretation: One-Sensor Theory (OST) and Line-Labeled Theory (LLT). In OST, one afferent fiber connects to a single sensor. In LLT, a different type of sensor sends signals via its specific line to a particular brain region to evoke its reflex. Thus, airway slowly adapting receptors (SARs) inhibit breathing and rapidly adapting receptors (RARs) stimulate breathing. However, recent studies show many different mechanosensors connect to a single afferent fiber (Multiple-Sensor Theory, MST). That is, SARs and RARs may send different types of information through the same afferent pathway, indicating different information has been integrated at the sensory unit level. Thus, a sensory unit is not merely a transducer (textbook concept), but also a processor. MST is a conceptual shift. Data generated over last eight decades under OST require re-interpretation. • Airway mechanosensors play an important role in respiratory control and other body function. • Recent research advances a paradigm shifting multiple-sensor theory to explain the mechanosensory function. • It overviews derivation of MST. • MST provides new data interpretation; for instance, coughs can arise from activating four sensor types together in the unit. [ABSTRACT FROM AUTHOR]

Mechanosensing and subsequent mechanotransduction are indispensable for muscle plasticity. Nevertheless, a scarcity of literature exists regarding an all-encompassing understanding of the muscle mechanosensing machinery's response to prolonged loading, especially in conditions that resemble a natural physiological state of skeletal muscle. This study aimed to comprehensively explore the effects of prolonged mechanical loading on mechanosensitive components, skeletal muscle characteristics, and metabolism-related gene clusters. Twenty male C57BL/6J mice were randomly divided into two groups: control and prolonged mechanical loading. To induce prolonged mechanical loading on the triceps brachii (TRI) and biceps brachii (BIC) muscles, a 14-day period of tail suspension was implemented. In TRI only, prolonged mechanical loading caused a mild fast-to-slow fiber type shift together with increased mechanosensor gene and protein levels. It also increased transcription factors associated with slow muscle fibers while decreasing those related to fast-type muscle gene expression. Succinate dehydrogenase activity, a marker of muscle oxidative capacity, and genes involved in oxidative and mitochondrial turnover increased, whereas glycolytic-related genes decreased. Moreover, prolonged mechanical loading stimulated markers of muscle protein synthesis. Taken together, our data show a collective muscle-specific increase in mechanosensor gene and protein levels upon a period of prolonged mechanical loading in conditions that reflect a more natural physiological state of skeletal muscle in mice. We provide additional proof-of-concept that prolonged tail suspension-induced loading of the forelimbs triggers a muscle-specific fast-to-slow fiber type switch, and this coincides with increased protein synthesis-related signaling. NEW & NOTEWORTHY This study provides a comprehensive overview of the effects of prolonged loading on mechanosensitive components in conditions that better reflect the natural physiological state of skeletal muscle. Although the muscle mechanosensing machinery has been widely acknowledged for its responsiveness to altered loading, an inclusive understanding of its response to prolonged loading remains scarce. Our results show a fast-to-slow fiber type shift and an upregulation of mechanosensor gene and protein levels following prolonged loading.

The fruit fly Drosophila melanogaster has provided important insights into how sensory information is transduced by transient receptor potential (TRP) channels in the peripheral nervous system (PNS). However, TRP channels alone have not been able to completely model mechanosensitive transduction in mechanoreceptive chordotonal neurons (CNs). Here, we show that, in addition to TRP channels, the sole voltage-gated sodium channel (Na V ) in Drosophila , Para, is localized to the dendrites of CNs. Para is localized to the distal tip of the dendrites in all CNs, from embryos to adults, and is colocalized with the mechanosensitive TRP channels No mechanoreceptor potential C (NompC) and Inactive/Nanchung (Iav/Nan). Para localization also demarcates spike initiation zones (SIZs) in axons and the dendritic localization of Para is indicative of a likely dendritic SIZ in fly CNs. Para is not present in the dendrites of other peripheral sensory neurons. In both multipolar and bipolar neurons in the PNS, Para is present in a proximal region of the axon, comparable to the axonal initial segment (AIS) in vertebrates, 40-60 μm from the soma in multipolar neurons and 20-40 μm in bipolar neurons. Whole-cell reduction of para expression using RNAi in CNs of the adult Johnston's organ (JO) severely affects sound-evoked potentials (SEPs). However, the duality of Para localization in the CN dendrites and axons identifies a need to develop resources to study compartment-specific roles of proteins that will enable us to better understand Para's role in mechanosensitive transduction., Competing Interests: The authors declare no competing financial interests., (Copyright © 2023 Ravenscroft et al.)

Background Lipoprotein lipase (LPL)-derived fatty acid is a major source of energy for cardiac contraction. Synthesized in cardiomyocytes, LPL requires translocation to the vascular lumen for hydrolysis of lipoprotein triglyceride, an action mediated by endothelial cell (EC) release of heparanase. We determined whether flow-mediated biophysical forces can cause ECs to secrete heparanase and thus regulate cardiac metabolism. Methods and Results Isolated hearts were retrogradely perfused. Confluent rat aortic ECs were exposed to laminar flow using an orbital shaker. Cathepsin L activity was determined using gelatin-zymography. Diabetes was induced in rats with streptozotocin. Despite the abundance of enzymatically active heparanase in the heart, it was the enzymatically inactive, latent heparanase that was exceptionally responsive to flow-induced release. EC exposed to orbital rotation exhibited a similar pattern of heparanase secretion, an effect that was reproduced by activation of the mechanosensor, Piezo1. The laminar flow-mediated release of heparanase from EC required activation of both the purinergic receptor and protein kinase D, a kinase that assists in vesicular transport of proteins. Heparanase influenced cardiac metabolism by increasing cardiomyocyte LPL displacement along with subsequent replenishment. The flow-induced heparanase secretion was augmented following diabetes and could explain the increased heparin-releasable pool of LPL at the coronary lumen in these diabetic hearts. Conclusions ECs sense fluid shear-stress and communicate this information to subjacent cardiomyocytes with the help of heparanase. This flow-induced mechanosensing and its dynamic control of cardiac metabolism to generate ATP, using LPL-derived fatty acid, is exquisitely adapted to respond to disease conditions, like diabetes.

Ligand-receptor interactions guide axon navigation and dendrite arborization. Mechanical forces also influence guidance choices. However, the nature of such mechanical stimulations, the mechanosensor identity, and how they interact with guidance receptors are unknown. Here, we demonstrate that mechanosensitive DEG/ENaC channels are required for dendritic arbor morphogenesis in Caenorhabditis elegans. Inhibition of DEG/ENaC channels causes reduced dendritic outgrowth and branching in vivo , a phenotype that is alleviated by overexpression of the mechanosensitive channels PEZO-1/Piezo or YVC1/TrpY1. DEG/ENaCs trigger local Ca2+ transients in growing dendritic filopodia via activation of L-type voltage-gated Ca2+ channels. Anchoring of filopodia by dendrite ligand-receptor complexes is required for the mechanical activation of DEG/ENaC channels. Therefore, mechanosensitive channels serve as a checkpoint for appropriate chemoaffinity by activating Ca2+ transients required for neurite growth. [Display omitted] • The mechanosensitive DEG/ENaC channels are activated during dendrite outgrowth • DEG/ENaC channels activate voltage-gated Ca2+ channels to promote dendrite growth • DEG/ENaC channels shape dendrite arbors by validating ligand-receptor interactions Tao and Coakley et al. show that the force experienced by growing neurites is sufficient to activate ion channels that sense touch. Once activated, these channels further promote and fine-tune the outgrowth of dendrites. Together, these results define a role for mechanosensitive channels in shaping dendritic arbors during neuronal development. [ABSTRACT FROM AUTHOR]

Nature has created high-performance materials and structures over millions of years of evolution. Inspired by the concepts and design principles evident in natural materials and structures, high-performance tactile sensors, based on bioinspired structures/functions, natural biopolymers, and biomimetic strategies, have been developed. However, the primary challenge is to develop novel sensing mechanisms and device structures that are sufficiently sensitive and stretchable using bioinspired materials. Herein, we review the recent advancements made in this field, focusing on biomimetic approaches to produce tactile sensors with essential sensing capabilities and the development of bioinspired materials with the desired electrical and mechanical properties. In addition, we highlight the potential applications of these devices and discuss the potential directions for future work. [ABSTRACT FROM AUTHOR]