Apoptosis, the genetically programmed suicide, plays a critical role in a number of physiological and pathological cell conditions. Several molecules and signaling pathways involved in apoptosis have been recently identified and many of them are well characterized. However, the role of cytosolic organelles and their interactions during apoptosis is unknown and requires further investigation. In some reports, cytosolic organelles including the mitochondria, endoplasmic reticulum, Golgi apparatus, peroxisome, lysosome and nucleus are recognized as the members of a “third pathway” of apoptosis. This pathway is considered completely different from the intrinsic and extrinsic pathways of apoptosis. The present paper will review the function of several cytosolic organelles separately, and discuss the importance of the third pathway of apoptosis.

Background: In the ovary, growing follicles develop from a pool of primordial follicles constituted early in life. The majority of ovarian follicles undergo atresia. Follicular atresia is an important and negative process during the development of ovarian follicles. Cell apoptosis is believed to be involved in this process. This article is an overview of some researches on apoptosis in the ovaries and the factors involved in it. Materials and Methods: In this review article, the PubMed, Scopus, Embase, Current Content, and IranMedex databases were searched using keywords such as "apoptosis" and "ovary". The full-text articles published between 1997 and 2017 in English or Persian were included in the study. The genes involved in ovarian apoptosis and factors controlling follicle atresia and their role in ovarian follicular reserve and fertility were investigated. Results: Although follicular atresia occurs at all stages of follicular development, it has been shown that this process is dependent on the developmental stage and a large part of it is observed in the transitional stage between the preantral follicles and the antrum formation. Different paracrine and autocrine factors control the cell death of the ovary. Conclusion: Ovarian cells receive conflicting signals for survival and death, and it seems that the reason for determining the fate of cells in different stages of follicular development is the interaction between different signals.

Neurodegenerative diseases cause a range of neurological disorders in the central nervous system. Todays researchers emphasize the pivotal role of apoptosis in neurodegenerative diseases. Given that injured central nervous system has limited regenerative capacity, it is of extreme importance to limit the damage by inhibition of neuronal death. During the past decade, considerable progress has been made in understanding the process of apoptosis at molecular level. Also, according to the understanding of the mechanisms of apoptosis, several studies have examined the possible effects of neuroprotective compounds for reducing or inhibiting neuronal apoptosis. In this review article, it has been attempt to review the role of apoptosis in the pathology of neurodegenerative diseases. Also, an overview has been made in the field of neuronal apoptosis inhibitor with neuroprotective compounds in human and experimental models of neurodegenerative diseases.

Introduction: P53 is the most famous tumor suppressor gene that is mutated in over 50% of human cancers. This gene has been described as "guardian of the genome"," the guardian angel gene", and the " master watchman", referring to its critical role in genomic stability, and tumor suppression mainly by inducing apoptosis, cell cycle arrest, and senescence, inhibition of angiogenesis. In this review article were discussed recent advances in p53 research, mainly its role in apoptosis and the approaches to target p53 and its regulators for cancer treatment aimed to either to activate p53 in cancer cells to kill them or temporarily inactivation of p53 in the normal cells to protect them against chemo-radiation.Conclusion: Due to the vital roles of P53 in carcinogenesis inhibition, this protein is one of the most important therapeutic targets for cancer therapy. Based on genetic variation type in P53, in the normal and tumor cells, a combination of different therapies can be used and also by more comprehensive consideration of the involved signaling pathways new upstream and downstream novel proteins can be discovered to act as targets for new therapeutic targets.

Cancer is a complex and life-threatening disease involving uncontrollable cell proliferation, evading apoptosis, and metastasis. Despite recent developments in cancer chemotherapy, there are no effective broad spectrum anticancer agents that could selectively target cancer cells. Thus, designing and discovering new efficient and selective anticancer agents are urgent needs. It is important that new anticancer agents could act via apoptosis induction, since it has a critical role in control of cell proliferation. Chalcones are naturally occurring compounds possessing high degree of synthetic diversity for design of new leading bioactive compounds including anticancer agents. Chalcones are considered as promising anticancer agents against most human cancers with capability of inducing apoptosis in cancer cells. Furthermore, some clinically useful anticancer drugs show genotoxicity due to interaction with DNA, but chalcones with different mechanism may be devoid of this side effect. This review highlights the recently identified anticancer chalcones from naturally or synthetically origins that induce apoptosis in cancer cells. The diversity of scaffolds described in this review along with their structure-activity relationships could help medicinal chemists in development of new selective anticancer chalcones with improved potency.