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Updated: May 24, 2026

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
Published on: September 3, 2020
Pressure overload leads to an increase of cardiac resident stem cells
Stefan Rupp1, Jürgen Bauer, Susanne von Gerlach
1Pediatric Heart Center, University of Giessen and Marburg, Feulgenstrasse 12, 35390, Giessen, Germany.
Insights
The mammalian heart has some regenerative capacity, particularly after injury. This study found a significant increase in cardiac resident stem cells in pressure-overloaded right ventricles, suggesting a potential repair mechanism.
Area of Science:
- Cardiovascular Biology
- Regenerative Medicine
- Cardiac Pathology
Background:
- Mammalian hearts exhibit limited regenerative potential, mainly observed postnatally and following injury like myocardial infarction or pressure overload.
- The specific cell types responsible for endogenous cardiac regeneration remain largely unidentified, with cardiac stem cells being a key area of investigation.
Purpose of the Study:
- To quantify the number of c-kit+ cardiac resident cells in human hearts subjected to pressure overload.
- To investigate the role of these cells in the context of cardiac stress and potential regenerative mechanisms.
Main Methods:
- Analysis of cardiac tissue specimens from patients with pressure-overloaded single right ventricles (n=8), dilated cardiomyopathy (n=4), and post-heart transplant biopsies (n=14).
- Quantification of c-kit+/mast cell tryptase-/CD45- cells, identified as putative cardiac stem cells, as a percentage of total nuclei.
- Comparison of cell counts across different patient groups, with patient ages ranging from 16 days to 19 years.
Main Results:
- A significantly higher proportion of c-kit+/mast cell tryptase-/CD45- cells (0.41 ± 0.24%) was detected in pressure-overloaded single right ventricles compared to dilated cardiomyopathy explants (0.13 ± 0.09%).
- This represents an approximately three-fold increase in these specific cardiac resident cells under pressure overload conditions.
- Despite the increase, the number of these cells was insufficient to prevent the progression to congestive heart failure.
Conclusions:
- Pressure overload in the right ventricle leads to a notable increase in c-kit+ cardiac resident cells.
- Understanding the mechanisms driving this stem cell increase could pave the way for novel therapeutic strategies to enhance cardiac repair.
- While these cells are implicated in a regenerative response, their current numbers do not fully counteract the detrimental effects of severe cardiac pressure overload.
Abstract:
Recent studies suggest that the mammalian heart possesses some capacity for cardiac regeneration. This regenerative capacity is primarily documented postnatally and after myocardial infarction or pressure overload. Although the cell type that mediates endogenous regeneration is unclear, cardiac stem cells might be considered as potential candidates. To determine the number of c-kit + cardiac resident cells under conditions of pressure overload, we evaluated specimens derived from n = 8 patients with pressure overloaded single right ventricles in comparison to n = 4 explanted hearts from patients with dilated cardiomyopathy and n = 14 biopsies from children after heart transplantation. The age of the patients ranged from 16 days to 19 years. For quantification of cardiac stem cells, c-kit+/mast cell tryptase-/CD45- cells were counted and expressed as percent of the total nuclei. In specimens from patients with dilated cardiomyopathy, 0.13 ± 0.09% c-kit +/mast cell tryptase-/CD45- cells were detected. However, in specimens from patients with pressure overloaded single right ventricles, the numbers of c-kit+/mast cell tryptase-/CD45- cells were significantly higher (0.41 ±0.24%, p < 0.05). Under conditions of pressure overload, the right ventricle shows an approximately three-fold increase in c-kit+/mast cell tryptase-/CD45- cardiac resident cells. Despite the fact that this increased number of c-kit+ cells is not sufficient to prevent the failing heart from congestive heart failure, understanding the mechanism that leads to an increase of presumably cardiac resident stem cells under conditions of pressure overload might help to develop new strategies to enhance endogenous repair.
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