 Mitotic catastrophe is a type of cell death that occurs during mitosis. It results from a combination of cellular damage and malfunction of several cell-cycle checkpoints such as the G1, S, and G2 DNA-damage checkpoints or the spindle-assembly checkpoint (page 87). Failure to arrest the cell cycle before mitosis occurs causes problems with chromosome separation, which triggers the apoptotic pathway and cell death.
 Paraptosis is an alternative, nonapoptotic cell death that may be induced by growth factor receptors (i.e., insulin growth factor [IGF-1] receptor). In contrast to apoptosis, cell death is not mediated by caspases but by mitogenactivated protein kinases (MAPKs). On a cellular level, paraptosis is characterized by the formation of multiple large vacuoles within the cell cytoplasm along with mitochondrial swellings.
 Pyroptosis is a form of cell death induced by infection with certain microorganisms that generate intense inflammatory reactions. This pathway is uniquely dependent on the caspase-1 enzyme, which is not involved in caspase cascade in apoptotic cell death. Caspase-1 activates the inflammatory cytokines such as IL-1 and IL-18 that mediate intense inflammatory reactions in surrounding tissue.
 Necroptosis is a regulated caspase-independent cell death mechanism that can be induced in different cell types. It is initiated by the activation of the tumor necrosis factor receptors (TNFRs or death receptors) and Fas signaling pathway. Although it occurs under regulated conditions, necroptotic cell death is characterized by the same morphologic features as unregulated necrotic death. Necrostatin-1 is a specific inhibitor of necroptosis that significantly reduces ischemic damage in affected tissues.
FIGURE 3.20 • Schematic drawing of mechanisms leading to apoptosis. Both external and internal stimuli can trigger apoptosis by activating the enzymatic caspase cascade. Many external activators act on the cell to initiate signals leading to apoptosis; note that TNF and TGFact through a “death receptor.” Controlled release of cytochrome c from mitochondria is an important internal step in the activation of apoptosis.
Microscopic studies of dying cells in the tissue reveals that different forms of cell death can occur simultaneously and that dying cells can share features of different types of cell death.
Tissues: Concept and Classification
OVERVIEW OF TISSUES / 98 EPITHELIUM / 99 CONNECTIVE TISSUE / 99 MUSCLE TISSUE / 100 NERVE TISSUE / 101 HISTOGENESIS OF TISSUES / 102 Ectodermal Derivatives / 102 Mesodermal Derivatives / 102 Endodermal Derivatives / 102 IDENTIFYING TISSUES / 102 Folder 4.1 Clinical Correlation: Ovarian Teratomas / 103
Tissues are aggregates or groups of cells organized to perform one or more specific functions.
At the light microscope level, the cells and extracellular components of the various organs of the body exhibit a recognizable and often distinctive pattern of organization. This organized arrangement reflects the cooperative effort of cells performing a particular function. Therefore, an organized aggregation of cells that function in a collective manner is called a tissue [Fr. tissu, woven; L. texo, to weave].
Although it is frequently said that the cell is the basic functional unit of the body, it is really the tissues, through the collaborative efforts of their individual cells, that are responsible for maintaining body functions. Cells within tissues communicate through specialized intercellular junctions (gap junctions, page 131), thus facilitating this collaborative effort and allowing the cells to operate as a functional unit. Other mechanisms that permit the cells of a given tissue to function in a unified manner include specific membrane receptors and anchoring junctions between cells.