Key result
Atorvastatin reduces α-SMA, GATA4, and MEF2C expression while increasing fibrosis-related microRNAs in human cardiac fibroblasts.
Why the study?
Cardiac fibroblast activation into myofibroblasts drives cardiac fibrosis, making strategies to reverse or inhibit this phenotypic transition of critical interest.
Does atorvastatin reduce myofibroblast activation in primary human cardiac fibroblasts?
Does atorvastatin reduce myofibroblast activation in primary human cardiac fibroblasts?
Atorvastatin attenuates human cardiac fibroblast activation in vitro, highlighting potential transcriptional and post-transcriptional regulatory mechanisms for its anti-fibrotic effects.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for atorvastatin in cardiac fibrosis; prospective trials needed before clinical adoption.
Cardiac fibroblast activation into α-smooth muscle actin (α-SMA)-expressing myofibroblasts is a central event in the progression of cardiac fibrosis. Therapeutic strategies capable of reversing or inhibiting this phenotypic transition are therefore of critical interest. Here, we explore associative changes in transcriptional and post-transcriptional regulators linked to fibroblast activation following atorvastatin exposure in primary human cardiac fibroblasts (HCFs). Atorvastatin treatment (10 µM) was associated with a reduction in α-SMA expression, consistent with decreased myofibroblast activation. This change co-occurred with reduced expression of the transcription factors GATA4 and MEF2C, which are implicated in cardiac cell identity and plasticity. Concurrently, atorvastatin treatment was associated with selective increase in specific fibrosis-related microRNAs, including miR-24, miR-26a, and miR-133a, whereas the expression of miR-21 and miR-23a remained unchanged. Together, these findings describe a coordinated pattern of transcriptional and post-transcriptional changes associated with atorvastatin exposure in HCFs, consistent with a shift away from the myofibroblast phenotype. These observations provide descriptive, hypothesis-generating insight into potential regulatory patterns associated with atorvastatin treatment, although further functional studies are required to establish causal relationships and translational relevance.
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Chomaničová et al. (2026) studied Cardiac fibrosis. Atorvastatin was evaluated on α-SMA expression, GATA4 and MEF2C expression, and fibrosis-related microRNAs. Atorvastatin treatment (10 µM) in primary human cardiac fibroblasts reduced α-SMA, GATA4, and MEF2C expression while increasing specific fibrosis-related microRNAs (miR-24, miR-26a, miR-133a).
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