The cardiovascular system plays a crucial role in the entire organism. It performs many important functions, such as providing organs and tissues with nutrients, hormones, delivering oxygen to cells, and maintaining physiological temperature. For a long time, accurately identifying the nonlinear and anisotropic mechanical properties of the vascular wall within the body has been regarded as a key challenge in cardiovascular biomechanics, as these properties are critical determinants of overall cardiac function. Currently, the roles of mechanical and tissue properties in cardiovascular diseases such as arterial aneurysms and atherosclerosis remain hot topics in both basic and clinical researches. This review aims to summarize the latest research advances in the field of cardiovascular biomechanics and mechanobiology in the year 2022. In terms of cardiovascular biomechanics, researchers focus on the structure, function, and pathophysiology of the cardiovascular system, and use experimental methods such as mechanical modeling to study these issues. These include studies about biomechanical properties of diseases such as atherosclerosis, arterial aneurysms, and myocardial infarction, as well as the development and testing of treatment methods based on dynamics of the cardiovascular system. In terms of mechanobiology, researchers explore mechanical properties of cardiovascular cells and extracellular matrix, including prediction of cell mechanical properties based on machine learning, studies of biological material mechanical properties, and the role of mechanical properties in cardiovascular cell phenotype changes. These research findings provide new ideas and methods for diagnosing and treating cardiovascular diseases and offer new insights into researches in biomechanics and mechanobiology fields.

Calnexin is a lectin-like molecular chaperone protein on the endoplasmic reticulum, mediating unfolded protein responses, the endoplasmic reticulum Ca homeostasis, and Ca signals conduction. In recent years, studies have found that calnexin plays a key role in the heart diseases. This study aims to explore the role of calnexin in the activation of cardiac fibroblasts. A transverse aortic constriction (TAC) mouse model was established to observe the activation of cardiac fibroblasts , and the cardiac fibroblasts activation model was established by transforming growth factor β1 (TGFβ1) stimulation. The adenovirus was respectively used to gene overexpression and silencing calnexin in cardiac fibroblasts to elucidate the relationship between calnexin and cardiac fibroblasts activation, as well as the possible underlying mechanism. We confirmed the establishment of TAC model by echocardiography, hematoxylin-eosin, Masson, and Sirius red staining, and detecting the expression of cardiac fibrosis markers in cardiac tissues. After TGFβ1 stimulation, markers of the activation of cardiac fibroblast, and proliferation and migration of cardiac fibroblast were detected by quantitative PCR, Western blot, EdU assay, and wound healing assay respectively. The results showed that the calnexin expression was reduced in both the TAC mice model and the activated cardiac fibroblasts. The overexpression of calnexin relieved cardiac fibroblasts activation, in contrast, the silencing of calnexin promoted cardiac fibroblasts activation. Furthermore, we found that the endoplasmic reticulum stress was activated during cardiac fibroblasts activation, and endoplasmic reticulum stress was relieved after overexpression of calnexin. Conversely, after the silencing of calnexin, endoplasmic reticulum stress was further aggravated, accompanying with the activation of cardiac fibroblasts. Our data suggest that the overexpression of calnexin may prevent cardiac fibroblasts against activation by alleviating endoplasmic reticulum stress.

Long non-coding RNA (lncRNA) Dnm3os plays a critical role in peritendinous fibrosis and pulmonary fibrosis, but its role in the process of cardiac fibrosis is still unclear. Therefore, we carried out study by using the myocardial fibrotic tissues obtained by thoracic aortic constriction (TAC) in an early study of our group, and the
Fibroblasts ; Fibrosis ; Humans ; Myocardium/pathology* ; RNA, Long Noncoding ; Signal Transduction ; Transforming Growth Factor beta1