Inhibition of stress-activated p38 mitogen-activated protein kinase induces low-density lipoprotein receptor expression

Trends Cardiovasc Med. 1999 Oct;9(7):201-5. doi: 10.1016/s1050-1738(00)00021-9.


We have recently shown that different signal transduction pathways initiated by a variety of agents converge on growth-responsive p42/44MAPK signaling cascade to induce low-density lipoprotein (LDL) receptor expression. Our recent demonstration that stress-activated p38MAPK negatively regulates LDL receptor expression in an isoform-specific manner via modulation of p42/44MAPK cascade represents a new dimension of complexity in the molecular communication that governs LDL receptor expression. The suggested one-way communication between p38MAPK and p42/44MAPK provides a potential mechanism for fine-tuning cellular levels of cholesterol in response to a diverse set of environmental cues, including stress. Cross talk between MAPKs opens new avenues toward understanding a variety of pathogenic processes; this makes them tempting targets for therapeutic interventions in cardiovascular diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Enzyme Activation
  • Humans
  • Hypercholesterolemia / metabolism*
  • Hypercholesterolemia / physiopathology
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinases / metabolism*
  • Receptors, LDL / metabolism*
  • Signal Transduction
  • Stress, Psychological / physiopathology
  • p38 Mitogen-Activated Protein Kinases


  • Receptors, LDL
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases