Video Experimental Relacionado

Updated: Jan 8, 2026

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

Published on: October 26, 2015

Eventos adversos renales asociados con inhibidores de la quinasa dependiente de ciclina 4/6

Hassan Izzedine¹, Rimda Wanchoo², Ruby Sharma³

¹Department of Nephrology, Peupliers Private Hospital, Paris, France.

Cancer treatment reviews

|December 12, 2025

Resumen

Los inhibidores de la quinasa dependiente de ciclina 4/6 mejoran la supervivencia en el cáncer de mama pero pueden causar problemas renales, incluida lesión renal aguda verdadera y pseudo-AKI. La monitorización cuidadosa es esencial para el manejo de estos eventos adversos renales.

Área de la Ciencia:

Oncología; Nefrología; Farmacología

Sus antecedentes:

Los inhibidores de la quinasa dependiente de ciclina 4/6 (CDK4/6i) son un tratamiento estándar para el cáncer de mama HR+, HER2-, y mejoran la supervivencia.; Los eventos adversos asociados con los inhibidores de CDK4/6i afectan comúnmente los sistemas renal, cardiovascular y metabólico.; Las reacciones nefrotóxicas son más frecuentes con los inhibidores de CDK4/6i, y abemaciclib muestra un mayor riesgo.

Objetivo del estudio:

Revisar los eventos adversos renales asociados con los inhibidores de CDK4/6i en el tratamiento del cáncer de mama.; Diferenciar entre la lesión renal aguda verdadera y el pseudo-AKI causado por los inhibidores de CDK4/6i.; Destacar la importancia de monitorizar la función renal y manejar las interacciones farmacológicas.

Principales métodos:

Revisión de datos clínicos sobre inhibidores de CDK4/6i y eventos adversos renales.; Análisis de estudios preclínicos que investigan efectos renales a largo plazo.; Examen de interacciones farmacológicas y estrategias de monitorización.

Principales resultados:

Los inhibidores de CDK4/6i pueden causar LRA verdadera (lesión tubular aguda, nefritis intersticial) y pseudo-AKI (aumento de creatinina a través de la inhibición de OCT2/MATE).; El pseudo-AKI puede no reflejar una disminución real de la tasa de filtración glomerular (TFG), lo que requiere la evaluación de cistatina C.; Los estudios preclínicos a largo plazo muestran recuperación deteriorada, fibrosis y senescencia después de LRA isquémica con palbociclib.; También se observan hipertensión, desequilibrios electrolíticos e interacciones farmacológicas significativas.

Conclusiones:

La monitorización renal vigilante es crucial para los pacientes en terapia con inhibidores de CDK4/6i.; Se necesita un enfoque multidisciplinario para manejar los eventos adversos renales y de otro tipo.; La evaluación precisa de la TFG utilizando tanto creatinina como cistatina C es importante.

Palabras clave:

Cáncer de mama Inhibidores de CDK4/6 Nefrotoxicidad Onconefrlogía Pseudo AKI

Más Videos Relacionados

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

Videos de Conceptos Relacionados

Inhibition of Cdk Activity

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

M-Cdk Drives Transition Into Mitosis

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

Anaphase Promoting Complex

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...

Positive Regulator Molecules

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

Positive Regulator Molecules

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...