RESUMO
Plants have remarkable abilities to regenerate in response to wounding. How wounding triggers rapid signal transduction to induce a cellular response is a key topic for understanding the molecular mechanism of plant regeneration. An increasing body of evidence indicates that jasmonate, a hormone that is produced rapidly in response to wounding, plays multiple roles in different plant regeneration processes. In this review, we summarize recent advances on the roles of jasmonate in tissue repair, the formation of wound-induced callus, de novo organ regeneration, and somatic embryogenesis. Physiological and molecular analyses indicate that jasmonate can regulate stem cell activities, cell proliferation, cell fate transition, and auxin production, thereby contributing to plant regeneration. In addition, jasmonate is strictly controlled in plant cells via restriction of the jasmonate concentration and its signalling pathway in a spatial and temporal manner during regeneration. Overall, jasmonate acts as the hormone linking wounding to distinct types of regeneration in plants.
Assuntos
Proteínas de Arabidopsis , Arabidopsis , Proteínas de Arabidopsis/metabolismo , Arabidopsis/metabolismo , Reguladores de Crescimento de Plantas/metabolismo , Ácidos Indolacéticos/metabolismo , Plantas/metabolismo , Hormônios/metabolismo , Regulação da Expressão Gênica de PlantasRESUMO
OPINION STATEMENT: With the development of molecular biology and histology techniques, targeted therapy for non-small cell lung cancer (NSCLC) has emerged, which is highly effective and has marginal side effects. Epidermal growth factor receptor (EGFR) was the first driver gene discovered, whose three generations of therapeutic use have its characteristics and benefits in clinical practice. However, cardiovascular complications by EGFR-tyrosine kinase inhibitors (EGFR-TKIs) in preclinical studies have been increasingly reported, including heart failure, cardiomyopathy, and QT prolongation, among others. Cardiotoxicity of targeted drugs significantly affects the therapeutic effect of NSCLC and has become the second leading cause of death in NSCLC. The aim of the present review was to recognize the potential cardiotoxicity of third-generation targeted drugs in the treatment of NSCLC and their associated mechanisms to help clinicians identify and prevent it early in the treatment, minimize the cardiotoxicity of targeted drugs, and improve the therapeutic effect of patients.