Understanding the mechanistic potential of plant based phytochemicals in management of postmenopausal osteoporosis.

Postmenopausal osteoporosis, an epidemic disorder is defined as a loss in bone mineral density and a greater possibility of fractures in older women. It is a multifactorial disease under the control of various genetic, hormonal, and environmental factors. Insufficiency of estrogen hormone, leads to postmenopausal osteoporosis. Hormone replacement therapy (HRT), despite being the most effective treatment, it is associated with the risk of breast cancer and cardiovascular disorders. This review seeks to compile the most recent information on medicinal plants and natural compounds used to treat and prevent postmenopausal osteoporosis. Furthermore, the origin, chemical constituents and the molecular mechanisms responsible for this therapeutic and preventive effect are also discussed. Literature research was conducted using PubMed, Science direct, Scopus, Web of Science, and Google Scholar. Different plant extracts and pure compounds exerts their antiosteoporotic activity by inhibition of RANKL and upregulation of OPG. RANKL signaling regulates osteoclast formation, characterized by increased bone turnover and osteoprotegrin is a decoy receptor for RANKL thereby preventing bone loss from excessive resorption. In addition, this review also includes the chemical structure of bioactive compounds acting on NFκB, TNF α, RUNX2. In conclusion, we propose that postmenopausal osteoporosis could be prevented or treated with herbal products.

Cancer stem cell-derived exosome-induced metastatic cancer: An orchestra within the tumor microenvironment.

Although the mechanisms as well as pathways associated with cancer stem cell (CSC) maintenance, expansion, and tumorigenicity have been extensively studied and the role of tumor cell (TC)-derived exosomes in this process is well understood, there is a paucity of research focusing specifically on the functional mechanisms of CSC-derived exosomes (CSC-Exo)/-exosomal-ncRNAs and their impact on malignancy. This shortcoming needs to be addressed, given that these vesicular and molecular components of CSCs could have a great impact on the cancer initiation, progression, and recurrence through their interaction with other key tumor microenvironment (TME) components, such as MSCs/MSC-Exo and CAFs/CAF-Exo. In particular, understanding CSCs/CSC-Exo and its crosstalk with MSCs/MSC-Exo or CAFs/CAF-Exo that are associated with the proliferation, migration, differentiation, angiogenesis, and metastasis through an enhanced process of self-renewal, chemotherapy as well as radiotherapy resistance may aid cancer treatment. This review contributes to this endeavor by summarizing the characteristic features and functional mechanisms of CSC-Exo/MSC-Exo/CAF-Exo and their mutual impact on cancer progression and therapy resistance.