[신간의 별자리x] 우리/미술, 그리고 ‘슬픔의 박물관’

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

https://biblio.ugent.be/publication/8555786/file/8555788.pdf

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

https://www.gastrojournal.org/article/S0016-5085(08)00429-0/pdf

Mechanisms of Hepatic Fibrogenesis

The hepatic stellate cell has surprised and engaged physiologists, pathologists, and hepatologists for over 130 years, yet clear evidence of its role in hepatic injury and fibrosis only emerged following the refinement of methods for its isolation and characterization. The paradigm in liver injury of activation of quiescent vitamin A-rich stellate cells into proliferative, contractile, and fibrogenic myofibroblasts has launched an era of astonishing progress in understanding the mechanistic basis of hepatic fibrosis progression and regression. But this simple paradigm has now yielded to a remarkably broad appreciation of the cell's functions not only in liver injury, but also in hepatic development, regeneration, xenobiotic responses, intermediary metabolism, and immunoregulation. Among the most exciting prospects is that stellate cells are essential for hepatic progenitor cell amplification and differentiation. Equally intriguing is the remarkable plasticity of stellate cells, not only in their variable intermediate filament phenotype, but also in their functions. Stellate cells can be viewed as the nexus in a complex sinusoidal milieu that requires tightly regulated autocrine and paracrine cross-talk, rapid responses to evolving extracellular matrix content, and exquisite responsiveness to the metabolic needs imposed by liver growth and repair. Moreover, roles vital to systemic homeostasis include their storage and mobilization of retinoids, their emerging capacity for antigen presentation and induction of tolerance, as well as their emerging relationship to bone marrow-derived cells. As interest in this cell type intensifies, more surprises and mysteries are sure to unfold that will ultimately benefit our understanding of liver physiology and the diagnosis and treatment of liver disease.

/pdf/hepatic-stellate-cells-protean-multifunctional-and-enigmatic-1ctrvjmfhn.pdf

Hepatic Stellate Cells: Protean, Multifunctional, and Enigmatic Cells of the Liver

In 2009, the Nomenclature Committee on Cell Death (NCCD) proposed a set of recommendations for the definition of distinct cell death morphologies and for the appropriate use of cell death-related terminology, including 'apoptosis', 'necrosis' and 'mitotic catastrophe'. In view of the substantial progress in the biochemical and genetic exploration of cell death, time has come to switch from morphological to molecular definitions of cell death modalities. Here we propose a functional classification of cell death subroutines that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe. Moreover, we discuss the utility of expressions indicating additional cell death modalities. On the basis of the new, revised NCCD classification, cell death subroutines are defined by a series of precise, measurable biochemical features.

/pdf/molecular-definitions-of-cell-death-subroutines-q5g428rlyi.pdf

Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012

/pdf/les-antagonistes-du-recepteur-cb1-des-cannabinoides-une-47v6w6h26g.pdf

« Les antagonistes du récepteur CB1 des cannabinoïdes : une nouvelle approche pour le traitement de la fibrose hépatique / CB1 cannabinoid receptor antagonists: a novel approach for the treatment of liver fibrosis »

The present invention relates to selective CB2 agonists for use in the prevention or treatment of alcoholic liver disease and particularly alcoholic hepatic steatosis and liver inflammation, and pharmaceutical composition thereof.

Selective CB2 Receptor Agonists for Use in the Prevention or Treatment of Alcoholic Liver Disease

93 interleukin-10 released by m2 kupffer cells promotes m1 kupffer cell apoptosis: a novel protective mechanism against alcoholic liver disease

C105SR, a novel non-peptidic small-molecule cyclophilin inhibitor with potent mitoprotective and hepatoprotective properties in the context of hepatic ischemia/reperfusion injury

Fatima Teixeira-Clerc

Papers

« Les antagonistes du récepteur CB1 des cannabinoïdes : une nouvelle approche pour le traitement de la fibrose hépatique / CB1 cannabinoid receptor antagonists: a novel approach for the treatment of liver fibrosis »

Selective CB2 Receptor Agonists for Use in the Prevention or Treatment of Alcoholic Liver Disease

93 interleukin-10 released by m2 kupffer cells promotes m1 kupffer cell apoptosis: a novel protective mechanism against alcoholic liver disease

C105SR, a novel non-peptidic small-molecule cyclophilin inhibitor with potent mitoprotective and hepatoprotective properties in the context of hepatic ischemia/reperfusion injury

Reply: To PMID 23728734.