Macroautophagy/autophagy is a complex degradation process with a dual role in cell death that is influenced by the cell types that are involved and the stressors they are exposed to. Ferroptosis is an iron-dependent oxidative form of cell death characterized by unrestricted lipid peroxidation in the context of heterogeneous and plastic mechanisms. Recent studies have shed light on the involvement of specific types of autophagy (e.g. ferritinophagy, lipophagy, and clockophagy) in initiating or executing ferroptotic cell death through the selective degradation of anti-injury proteins or organelles. Conversely, other forms of selective autophagy (e.g. reticulophagy and lysophagy) enhance the cellular defense against ferroptotic damage. Dysregulated autophagy-dependent ferroptosis has implications for a diverse range of pathological conditions. This review aims to present an updated definition of autophagy-dependent ferroptosis, discuss influential substrates and receptors, outline experimental methods, and propose guidelines for interpreting the results.Abbreviation: 3-MA:3-methyladenine; 4HNE: 4-hydroxynonenal; ACD: accidentalcell death; ADF: autophagy-dependentferroptosis; ARE: antioxidant response element; BH2:dihydrobiopterin; BH4: tetrahydrobiopterin; BMDMs: bonemarrow-derived macrophages; CMA: chaperone-mediated autophagy; CQ:chloroquine; DAMPs: danger/damage-associated molecular patterns; EMT,epithelial-mesenchymal transition; EPR: electronparamagnetic resonance; ER, endoplasmic reticulum; FRET: Försterresonance energy transfer; GFP: green fluorescent protein;GSH: glutathione;IF: immunofluorescence; IHC: immunohistochemistry; IOP, intraocularpressure; IRI: ischemia-reperfusion injury; LAA: linoleamide alkyne;MDA: malondialdehyde; PGSK: Phen Green™ SK;RCD: regulatedcell death; PUFAs: polyunsaturated fatty acids; RFP: red fluorescentprotein;ROS: reactive oxygen species; TBA: thiobarbituricacid; TBARS: thiobarbituric acid reactive substances; TEM:transmission electron microscopy.

This review focuses on oxidative stress and more specifically lipid peroxidation in cardiac surgery, one of the fundamental theories of perioperative complications. We present the molecular pathways leading to lipid peroxidation and integrate analytical methods that allow detection of lipid peroxidation markers in the fluid phase with those focusing on volatile compounds in exhaled breath. In order to explore the accumulated data in the literature, we present a systematic review of quantitative analysis of malondialdehyde, a widely used lipid peroxidation product at various stages of cardiac surgery. This exploration reveals major limitations of existing studies in terms of variability of reported values and significant gaps due to discrete and variable sampling times during surgery. We also appraise methodologies that allow real-time and continuous monitoring of oxidative stress. Complimentary techniques highlight that beyond the widely acclaimed contribution of the cardiopulmonary bypass technology and myocardial reperfusion injury, the use of diathermy contributes significantly to intraoperative lipid peroxidation. We conclude that there is an urgent need to implement the theory of oxidative stress towards a paradigm change in the clinical practice. Firstly, we need to acquire definite and irrefutable information on the link between lipid peroxidation and post-operative complications by building international consensus on best analytical approaches towards generating qualitatively and quantitatively comparable datasets in coordinated multicentre studies. Secondly, we should move away from routine low-risk surgeries towards higher risk interventions where there is major unmet clinical need for improving patient journey and outcomes. There is also need for consensus on best therapeutic interventions which could be tested in convincing large scale clinical trials. As future directions, we propose combination of fluid phase platforms and \'metabography\', an extended form of capnography-including real-time analysis of lipid peroxidation and volatile footprints of metabolism-for better patient phenotyping prior to and during high risk surgery towards molecular prediction, stratification and monitoring of the patient\'s journey.

Leaf senescence is not a chaotic breakdown but a dynamic process following a precise timetable. It enables plants to economize with their resources and control their own viability and integrity. The onset as well as the progression of leaf senescence are co-ordinated by a complex genetic network that continuously integrates developmental and environmental signals such as biotic and abiotic stresses. Therefore, studying senescence requires an integrative and multi-scale analysis of the dynamic changes occurring in plant physiology and metabolism. In addition to providing an automated and standardized method to quantify leaf senescence at the macroscopic scale, we also propose an analytic framework to investigate senescence at physiological, biochemical, and molecular levels throughout the plant life cycle. We have developed protocols and suggested methods for studying different key processes involved in senescence, including photosynthetic capacities, membrane degradation, redox status, and genetic regulation. All methods presented in this review were conducted on Arabidopsis thaliana Columbia-0 and results are compared with senescence-related mutants. This guideline includes experimental design, protocols, recommendations, and the automated tools for leaf senescence analyses that could also be applied to other species.