Mechanism of liponecrosis, a distinct mode of programmed cell death

Abstract

y These authors contributed equally to this work.

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

“…It is important to note that a stress/stimulus can in many circumstances induce different cell death pathways at the same time, which might lead to a "type" of cell death with mixed phenotypes. 1088,1089 Furthermore, inhibition of one cell death pathway (e.g., apoptosis) can either induce the compensatory activation of a secondary mechanism (e.g., necrosis), 1090,1091 or attenuate a primary mechanism (e.g., liponecrosis). 1088 The role of autophagy in the death of plant cells is less ambiguous, because plants are devoid of the apoptotic machinery and use lytic vacuoles to disassemble dying cells from inside.…”

“…1088,1089 Furthermore, inhibition of one cell death pathway (e.g., apoptosis) can either induce the compensatory activation of a secondary mechanism (e.g., necrosis), 1090,1091 or attenuate a primary mechanism (e.g., liponecrosis). 1088 The role of autophagy in the death of plant cells is less ambiguous, because plants are devoid of the apoptotic machinery and use lytic vacuoles to disassemble dying cells from inside. 1092 This mode of cell death governs many plant developmental processes and was named "vacuolar cell death".…”

Mechanisms by Which Different Functional States of Mitochondria Define Yeast Longevity

“…A lifespan checkpoint at which several distinct traits of mitochondrial functionality and homeostasis are linked to an age-related “liponecrotic” form of PCD is called checkpoint 7; it exists in ST growth phase [ 19 , 20 , 210 , 211 ]. These traits include (1) the efficiency with which mitochondria generate energy needed for the detoxification of non-esterified fatty acids through their incorporation into neutral lipids; an age-related decline in such efficiency accelerates age-related liponecrotic PCD by causing the excessive accumulation of monounsaturated fatty acids in cellular membranes; (2) the efficiencies with which mitochondria produce and release ROS; an age-related rise in such efficiencies above a threshold accelerates age-related liponecrotic PCD by causing oxidative damage to cellular macromolecules and organelles; and (3) the efficiency with which aged and dysfunctional mitochondria undergo an Atg32- and Aup1-driven selective autophagic degradation; an age-related decline in such efficiency accelerates age-related liponecrotic PCD by impairing the maintenance of a healthy population of fully functional mitochondria [ 18 , 19 , 20 , 158 , 159 , 182 , 210 , 211 , 212 , 213 , 214 , 215 ] ( Figure 3 ).…”

Squalene lipotoxicity in a lipid droplet‐less yeast mutant is linked to plasma membrane dysfunction

“…Similarly, cellular targets and mechanisms involved in the phenomenon of lipotoxicity are very similar in yeast and human cells ranging from changes in membrane properties, to oxidative stress, to mitochondrial dysfunction or endoplasmic reticulum stress. All these mechanisms typically converge in lipoapoptosis or liponecrosis (Kohlwein, ; Richard et al, ). Moreover, yeast and human cells utilize similar mechanisms of protection from lipotoxicity, most importantly seclusion of potentially toxic lipid species in lipid droplets (LD).…”

“…Similarly, cellular targets and mechanisms involved in the phenomenon of lipotoxicity are very similar in yeast and human cells ranging from changes in membrane properties, to oxidative stress, to mitochondrial dysfunction or endoplasmic reticulum stress. All these mechanisms typically converge in lipoapoptosis or liponecrosis (Kohlwein, 2010;Richard et al, 2014).…”