@entity65 and @entity5 continue to be major causes of @entity204 worldwide, and despite intensive research only modest progress has been reached in reducing the morbidity and mortality of these awful diseases. Mitochondria are broadly accepted as the key organelles that play a crucial role in cell life and @entity204 . They provide cells with @entity855 produced via oxidative phosphorylation under physiological conditions, and initiate cell @entity204 through both apoptosis and @entity39 in response to severe stress. Oxidative stress accompanied by @entity460 overload and @entity855 depletion induces the mitochondrial permeability transition (mPT) with formation of pathological, non-specific mPT pores ( @entity26508 ) in the mitochondrial inner membrane. Opening of the @entity26508 with a high conductance results in matrix swelling ultimately inducing @entity397 of the mitochondrial outer membrane and releasing pro-apoptotic proteins into the cytoplasm. The @entity855 level is the determining factor in deciding whether cells die through apoptosis or @entity39 . Cardiac cells undergoing @entity63 followed by reperfusion (IR) possess exactly the same conditions mentioned above to induce @entity26508 opening. Due to its critical role in cell @entity204 , inhibition of @entity26508 opening has been accepted as a major therapeutic approach to protect the heart against IR. In contrast to cardiac IR, @entity5 cells exhibit less sensitivity to pore opening which can be in part explained by increased expression of @entity26508 compounds/modulators and metabolic remodeling. Since the main goal of chemotherapy is to provoke apoptosis, mPT induction may represent an attractive approach for the development of new @entity5 therapeutics to induce mitochondria-mediated cell @entity204 and prevent cell differentiation in @entity105 . This review focuses on the role of the @entity26508 in cardiac IR and @entity5 , and pharmacological agents to prevent or initiate mPT-mediated cell @entity204 , respectively in these diseases.

Targeting the mitochondrial permeability transition: cardiac ischemia-reperfusion versus XXXX .

@entity39 :: ('MESH:D009336', 'Disease') :: ['necrosis'] @entity5 :: ('MESH:D009369', 'Disease') :: ['cancer'] @entity63 :: ('MESH:D007511', 'Disease') :: ['ischemia'] @entity397 :: ('MESH:D012421', 'Disease') :: ['rupture'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['calcium'] @entity105 :: ('MESH:D063646', 'Disease') :: ['carcinogenesis'] @entity26508 :: ('19273(Tax:10090)', 'Gene') :: ['mPTP'] @entity204 :: ('MESH:D003643', 'Disease') :: ['death'] @entity65 :: ('MESH:D002318', 'Disease') :: ['Cardiovascular diseases'] @entity855 :: ('MESH:D000255', 'Chemical') :: ['ATP']
@entity105 :: (MESH:D063646,Disease) :: ['carcinogenesis']
