[Anti remodeling therapy: new strategies and future perspective in post-ischemic heart failure. Part II]

Monaldi Arch Chest Dis. 2014 Dec;82(4):195-201. doi: 10.4081/monaldi.2014.64.
[Article in Italian]

Abstract

In recent years, the remarkable progress achieved in terms of survival after myocardial infarction have led to an increased incidence of chronic heart failure in survivors. This phenomenon is due to the still incomplete knowledge we possess about the complex pathophysiological mechanisms that regulate the response of cardiac tissue to ischemic injury. These involve various cell types such as fibroblasts, cells of the immune system, endothelial cells, cardiomyocytes and stem cells, as well as a myriad of mediators belonging to the system of cytokines and not only. In parallel with the latest findings on post-infarct remodeling, new potential therapeutic targets are arising to halt the progression of disease. After the evaluation of the results obtained from gene therapy and stem cells, in this part we evaluate micro-RNA, post-translational modification and microspheres based therapy.

Publication types

  • Review

MeSH terms

  • Genetic Therapy / methods*
  • HMGB1 Protein / genetics*
  • Heart Failure* / etiology
  • Heart Failure* / genetics
  • Heart Failure* / physiopathology
  • Heart Failure* / therapy
  • Humans
  • MicroRNAs* / classification
  • MicroRNAs* / genetics
  • Microspheres
  • Myocardial Infarction* / complications
  • Myocardial Infarction* / genetics
  • Myocardial Infarction* / physiopathology
  • Outcome Assessment, Health Care
  • RNA Processing, Post-Transcriptional / physiology
  • Stem Cell Transplantation / methods*
  • Ventricular Remodeling / genetics*

Substances

  • HMGB1 Protein
  • HMGB1 protein, human
  • MicroRNAs