Video Experimental Relacionado
Updated: Feb 20, 2026
06:52
Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
Published on: May 21, 2018
11.3K
Glucólisis y activación de la inflamación NLRP3 en enfermedades
Weijia Xu1,2, Xiaowen Zhu3, Qinghong Zhang2
1Department of Nephrology, Xuanwu Hospital, Capital Medical University, Changchun Street 45#, Beijing, 100053, People's Republic of China.
European journal of medical research
|February 19, 2026
Resumen
La reprogramación metabólica celular, específicamente la glucólisis, influye en la activación de la inflamación NLRP3. Esta revisión destaca el eje glucólisis-NLRP3 como un objetivo terapéutico para las enfermedades inflamatorias.
Área de la Ciencia:
- Metabolismo celular e inmunología.
- Vías de inflamación y muerte celular.
Sus antecedentes:
- La reprogramación metabólica es crucial para la adaptación y el destino celular.
- La inflamación NLRP3 impulsa la piroptosis y la inflamación.
- Existe una regulación recíproca entre la glucólisis y la activación de NLRP3.
Objetivo del estudio:
- Revisar la interacción entre la reprogramación glucolítica y la activación de la inflamación NLRP3.
- Elucidar los mecanismos de control metabólico sobre las vías de señalización inflamatoria.
Principales métodos:
- Revisión de la literatura sobre los avances recientes en reprogramación metabólica e investigación de inflamación.
- Síntesis de hallazgos sobre enzimas glucolíticas e intermedios metabólicos en la activación de NLRP3.
Principales resultados:
- Las enzimas glucolíticas (HK, PKM2) y el lactato modulan la activación de NLRP3.
- El eje glucólisis-NLRP3 vincula el control metabólico con la señalización inflamatoria.
Conclusiones:
- El eje glucólisis-NLRP3 es un regulador clave del destino celular en la inflamación.
- Dirigirse a este eje ofrece potencial terapéutico para patologías inflamatorias.
Videos de Conceptos Relacionados
01:38Inflammation
62.6K
Overview
62.6K
01:16Necrosis
6.8K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
6.8K
01:22Lysosomal Hydrolases
4.7K
Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
4.7K
01:24Caspases
14.3K
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
14.3K
01:18Autophagic Cell Death
4.7K
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
4.7K
01:31The Intrinsic Apoptotic Pathway
8.8K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
8.8K