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Cells & Development @cellsdev.bsky.social · 10/07/2026

Heart injuries can often be fatal, yet many animals can regenerate their 🫀 without leaving any scar, while others like 👨 cannot. Part of the reason lies in how the extracellular matrix is regulated. Patra et al discussed in details how this works and what we can learn from 🐟 doi.org/10.1016/j.cd...

Fig. 1. Zebrafish heart development stages illustrated from 5 h to 5 days post-fertilization

Fig. 2. Schematic representation of the major extracellular matrix (ECM) components and their interactions during heart development.

Fig. 3. Schematic of ECM-associated congenital heart defects in zebrafish (Table 1 & 3). (A) Denotes the wild-type scenario. (B and C) Lack of med10 or med12 caused reduced cardiac jelly, impairing valve formation. Additionally, med12 deficiency causes trabeculation defects (Just et al., 2016; Segert et al., 2018). (D) npnta morphants exhibit an expanded AV canal with increased cardiac jelly in both atrium and ventricles, impaired trabeculation, and defective AVC valves (Patra et al., 2011). Orange arrows indicate the atrioventricular canal, red arrows indicate blood flow direction, hpf; hours post fertilization, dpf; days post fertilization, V; ventricle, A; atrium, OFT; outflow tract.

Fig. 4. Heart regeneration in adult zebrafish (Table 2 & 3). (A) Distinct stages of heart regeneration after cryoinjury in wild-type adult zebrafish. Injury triggers regenerative responses immediately after injury, beginning with blood clot deposition and neocoronary angiogenesis. Followed by CM proliferation and infiltration along the neocoronaries into the wound. Post-injury, during the 1st and 2nd week, collagenous scar gets deposited in the injured tissue. As the heart continues to regenerate, the fibrotic scar gradually regresses. The regeneration process is completed by 90-120 days post cryoinjury, marked with minimal or no scar remaining. (B) Disruption of hapln1-expressing epicardial cells or hapln1b mutation in zebrafish impairs cardiomyocyte proliferation and heart regeneration (J. Sun et al., 2022). (C) Fn loss-of-function zebrafish mutants exhibit poor regeneration following myocardial injury, attributed to impaired CM migration; however, CM proliferation remains unaffected (J. Wang et al., 2013). (D) In ccn2a-/- injured hearts, while angiogenesis was observed, CM proliferation and repopulation were disrupted (Mukherjee et al., 2020). dpci; days post cryoinjury, dpi; days post-injury, OFT; outflow tract, CM; cardiomyocyte.

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