Immune cell dilemma in ischemic cardiomyopathy: to heal or not to heal

Sarita Nehra, Richard J. Gumina, Shyam S. Bansal

Research output: Contribution to journalReview articlepeer-review

8 Scopus citations


Inflammation is a double-edged sword for sterile tissue injury such as in myocardial infarction (MI). After ischemic injury, inflammatory immune responses activate repair processes, clear tissue-debris, form a stable scar and initiate angiogenesis in the myocardium for efficient wound-healing. However, incomplete immune resolution or sustained low-grade inflammation leads to ischemic cardiomyopathy (IC) characterized by maladaptive tissue remodeling and left-ventricular dilatation. It is clear that a delicate balance of cytokines, chemokines, prostaglandins, resolvins, and the innate and adaptive immune systems is critical for adequate healing as both insufficient-activation or overt-activation of inflammatory responses can either enhance rupture incidence or exacerbate cardiac dysfunction in the long-term. Among all the players, immune cells are the most critical as they are not only a source for all of the inflammatory protein mediators, but are also a target. However, phenotypic complexities associated with different immune subtypes, their inter-dependence, phasic-activations and varied functionalities often make it difficult to segregate the effects of one immune cell from another. In this review, we briefly summarize the role of several innate and adaptive immune cells to acquaint readers with complex immune-networks that dictate the extent of wound-healing post-MI and maladaptive remodeling during IC.

Original languageEnglish (US)
Pages (from-to)39-46
Number of pages8
JournalCurrent Opinion in Physiology
StatePublished - Feb 2021

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

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