Cellular and molecular mechanisms governing coral bleaching: Trends and implications

The molecular and cellular mechanisms that allow adult-stage neurons to regenerate following damage are poorly understood. Recently, axons of motoneurons and mechanosensory neurons in adult C. elegans were found to regrow after being snipped by femtosecond laser ablation. Here, we explore the molecular determinants of adult-stage axon regeneration using the AVM mechanosensory neurons. The first step in AVM axon development is a pioneer axonal projection from the cell body to the ventral nerve cord. We show that regeneration of the AVM axon to the ventral nerve cord lacks the deterministic precision of initial axon development, requiring competition and pruning of unwanted axon branches. Nevertheless, axons of injured AVM neurons regrow to the ventral nerve cord with over 60% reliability in adult animals. In addition, in contrast to initial development, axon guidance during regeneration becomes heavily dependent on cytoplasmic protein MIG-10/Lamellipodin but independent of UNC-129/TGF-beta repellent and UNC-40/DCC receptor, and axon growth during regeneration becomes heavily dependent on UNC-34/Ena and CED-10/Rac actin regulators. Thus, C. elegans may be used as a genetic system to characterize novel cellular and molecular mechanisms underlying adult-stage nervous system regeneration.

In this research topic, the primary focus is on understanding the cellular and molecular mechanisms in the pathogenesis of different neurodegenerative disorders. These include Alzheimer's disease (AD), Parkinson's disease (PD), and polyglutamine (polyQ) expansion diseases. To date, no cure exists for these disorders and it is paramount that research efforts continue to focus on understanding the molecular underpinnings behind these disorders. This will enable better symptom-directed therapeutics and perhaps even curative treatments to be developed.

HighlightsWhat are the main findings?Cardioplegia induces active molecular and cellular myocardial protection by regulating calcium handling, mitochondrial function, oxidative stress, and inflammatory pathways during cardiac arrest.Controlled cardioplegic arrest prolongs myocardial ischemic tolerance by suppressing electromechanical activity and reducing metabolic demand.What are the implications of the main findings?Mechanistic insights into cardioplegic protection support refinement of cardioplegia composition, temperature, and delivery strategies in CABG surgery.Optimization of cardioplegic protocols may improve postoperative myocardial recovery and reduce ischemia–reperfusion-related complications.Coronary artery bypass grafting (CABG) remains the gold standard for patients with advanced multivessel coronary artery disease. Optimal myocardial protection versus ischemia during reversible and controlled cardiac arrest is a cornerstone of successful outcomes. Myocardial ischemia represents a state of reduced coronary perfusion with oxygenated blood, insufficient to meet the metabolic demands of the myocardium. Conventional cardioplegic solutions offer controlled and reversible cardiac arrest while actively modulating the molecular and cellular mechanisms that mediate ischemia–reperfusion injury. Cardioplegia dramatically elongates the reversible period of ischemic injury and restricts cardiomyocyte death by shutting down electromechanical activity, lowering metabolic demand, stabilizing ionic homeostasis, protecting mitochondrial integrity, and slowing oxidative stress and inflammatory signaling. During ischemia, cardiomyocytes shift from aerobic to anaerobic metabolism, resulting in adenosine triphosphate (ATP) depletion, loss of ionic homeostasis and calcium overload that activate proteases, phospholipases and membrane damage. Reperfusion restores oxygen supply and prevents irreversible necrosis but paradoxically initiates additional injury in marginally viable myocardium. The reoxygenation phase induces excessive production of reactive oxygen species (ROS), endothelial dysfunction and a strong inflammatory response mediated by neutrophils, platelets and cytokines. Mitochondrial dysfunction and opening of the mitochondrial permeability transition pore (mPTP) further amplify oxidative stress and inflammation, and trigger apoptosis and necroptosis. Understanding these intertwined cellular and molecular mechanisms remains essential for identifying novel therapeutic targets aimed at reducing reperfusion injury and improving myocardial recovery after ischemic events, particularly in coronary surgery.

Molecular and cellular pruritus mechanisms in the host skin

Regulatory mechanisms and clinical manifestations of musculoskeletal aging.

The role of the Nrf2/Keap1 signaling cascade in mechanobiology and bone health

Microplastics (MPs) are pervasive environmental contaminants with significant bioaccumulation potential, posing a growing threat to global health through multi-organ toxicity. This review systematically synthesizes current knowledge on MPs-induced organ-specific damage and its systemic health implications. We detail the accumulation of MPs in major organ systems, including the liver, brain, lungs, kidneys, intestines, heart, and reproductive organs. Furthermore, we emphasize the critical role of inter-organ communication in amplifying toxicity, such as gut-liver axis-mediated hepatotoxicity and gut-brain axis-driven neurotoxicity. Emerging evidence on the transgenerational adverse effects of parental MPs exposure is also discussed. The core cellular and molecular mechanisms across these organs are examined, with a particular focus on oxidative stress, inflammatory activation, mitochondrial dysfunction, and programmed cell death. This review is distinct in its integrative approach, offering a novel perspective by synthesizing organ-specific pathologies with cross-organ communication networks and transgenerational effects, thereby providing a more holistic understanding of MPs' systemic toxicity. Collectively, this review elucidates the exposure-organ damage correlation, analyzes the underlying pathogenic mechanisms, and aims to provide a scientific foundation for public health risk assessment and informed environmental policy formulation.

P04. Dissecting the contribution of non-neural ectoderm to the vertebrate neural tube closure

International audience

Constructing explanations is essential for both science and learning. This study addresses the question, “What are the essential aspects of biology experts’ explanations of cellular and molecular mechanisms within their domain?” To address this question we first built on previous work and our own thought experiments to derive an initial model about mechanistic explanations. Secondly, we tested the validity of the initial model by asking seven biologists from various sub‐disciplines, to explain a cellular mechanism of their choice. Data was collected from interviews, artifacts and drawings and subjected to thematic analysis. We found that biologists: use our initial mechanistic model of molecular explanation by focusing on entities, activities, and organization. But in addition, they highly contextualize and constrain their explanations according to biological and societal significance; integrate explanations with the methods, instruments, and measurements they use to investigate; and use narrative stories along with analogies to explain their systems. These themes informed a modified model of expert‐like explanations of cellular mechanisms. Expert explanations consider four components: the Methods (M), Analogies (A), Context (C), and How (H) the mechanism works. Our model will provide a foundation for future work in life science education research, as well as other science domains, and offers a way to teach explicitly about components of biological mechanisms.

Thalamocortical axons must cross a complex cellular terrain through the developing forebrain, and this terrain has to be understood for us to learn how thalamocortical axons reach their destinations. Selective fasciculation, guidepost cells and various diencephalic and telencephalic gradients have been implicated in thalamocortical guidance. As our understanding of the relevant forebrain patterns has increased, so has our knowledge of the guidance mechanisms. Our aim here is to review recent observations of cellular and molecular mechanisms related to: the growth of thalamofugal projections to the ventral telencephalon, thalamic axon avoidance of the hypothalamus and extension into the telencephalon to form the internal capsule, the crossing of the pallial-subpallial boundary, and the growth towards the cerebral cortex. We shall review current theories for the explanation of the maintenance and alteration of topographic order in the thalamocortical projections to the cortex. It is now increasingly clear that several mechanisms are involved at different stages of thalamocortical development, and each contributes substantially to the eventual outcome. Revealing the molecular and cellular mechanisms can help to link specific genes to details of actual developmental mechanisms.

Static cold storage (SCS) on ice has remained the gold standard preservation method for heart transplantation, and prolonged cold ischemia outside the typical 4-6 hour window is associated with an increased risk of primary graft dysfunction - a consequence attributed to ischemic damage and reperfusion injury. This, unfortunately limits the travel radius for donor heart procurement, a key factor that contributes to the overall shortage of donor organs. Recent research and clinical data have illustrated the validity of other preservation systems in preserving cardiac allografts, and many of these devices have shown promise in potentially prolonging the tolerated ischemic time beyond the accepted standard. Unfortunately, little is known regarding the biological basis of these preservation systems. In this review, we explore the existing knowledge of ischemic reperfusion injury as it relates to the donor heart. We also focus on characterizing the cellular and molecular mechanisms underlying existing donor heart preservation methods, including SCS, Paragonix' SherpaPak, TransMedics' Organ Care System, and XVIVO Heart Perfusion System, highlighting current limitations and areas for improvement. Furthermore, we describe the preclinical and clinical heart transplant outcomes related to Hypothermic Oxygenated Perfusate (HOPE) preservation.

Cellular and molecular mechanisms of action of ovarian steroid hormones II: Regulation of sexual behavior in female rodents.

Chapter 11 - Chromoanagenesis phenomena and their formation mechanisms

Macrophage apoptosis is an important feature of atherosclerotic plaque development. Research directed at understanding the functional consequences of macrophage death in atherosclerosis has revealed opposing roles for apoptosis in atherosclerotic plaque progression. In early lesions, macrophage apoptosis limits lesion cellularity and suppresses plaque progression. In advanced lesions, macrophages apoptosis promotes the development of the necrotic core, a key factor in rendering plaques vulnerable to disruption and in acute lumenal thrombosis. The first section of this review will examine the role of phagocytic clearance of apoptotic macrophages, a process known as efferocytosis, in the dichotomous roles of macrophage apoptosis in early vs. advanced lesions. The second section will focus on the molecular and cellular mechanisms that are thought to govern macrophage death during atherosclerosis. Of particular interest is the complex and coordinated role that the endoplasmic reticulum (ER) stress pathway and pattern recognition receptors (PRRs) may play in triggering macrophage apoptosis.