What is the clinical evidence from this study?

Study design: Other. Population: Myocardial infarction. Intervention: FABP5 overexpression. Primary outcome: Cardiomyocyte cell cycle entry and cardiac function.

What does this research mean for the field?

Reactivating the RA/CD36/FABP5/PPARδ signaling axis via FABP5 overexpression drives adult cardiomyocyte cell-cycle re-entry and improves cardiac function following myocardial infarction. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To identify the molecular signaling pathway responsible for neonatal cardiomyocyte proliferation and determine whether reintroducing it into adult hearts can reactivate the cell cycle and promote cardiac regeneration.

September 19, 2026Cardiovascular ResearchOpen Access

Reintroducing FABP5 in adult mice drives cardiomyocyte cell cycle entry and improves post-MI cardiac function.

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Why the study?

Does reintroducing FABP5 induce cardiomyocyte cell cycle entry and improve cardiac function following myocardial infarction in adult mice?

Population

Mice models including P1 WT, CD36KO, CD36CKO, PPARδCTG, and inducible CM-specific FABP5 knock-in mice, as…

Comparison

Reintroduction of FABP5 in adult hearts using an… vs Control mice.

Design

Preclinical

Key result

Reintroducing FABP5 in adult mouse hearts drove cardiomyocyte cell cycle entry and significantly improved cardiac function following myocardial infarction.

Authors

ASAbou Bakr M. Salama QOQinghui Ou MDMarc Dwenger

Discussion

Member takes

Overview

Should not yet alter post-MI care; leaves open whether FABP5 reactivation promotes human cardiomyocyte regeneration.

Key Points

To identify the molecular signaling pathway responsible for neonatal cardiomyocyte proliferation and determine whether reintroducing it into adult hearts can reactivate the cell cycle and promote cardiac regeneration.
Characterized neonatal hearts from wild-type, CD36-knockout (CD36KO), and conditional CD36-knockout (CD36cKO) postnatal day 1 mice using single-cell and bulk RNA sequencing, spatial transcriptomics, and metabolomics.
Assessed retinoic acid signaling in CD36KO and FABP5 knockdown cardiomyocytes, and evaluated in vivo rescue by crossing CD36KO with cardiomyocyte-specific PPARδ overexpression.
Engineered an inducible cardiomyocyte-specific FABP5 knock-in mouse model to assess cell-cycle activation and cardiac functional recovery following myocardial infarction in adult mice.
Identified a CD36/FABP5/PPARδ axis enriched in proliferating neonatal cardiomyocytes, with CD36 knockout leading to a 50% reduction in retinoic acid levels and abolishing retinoic acid-induced proliferation.
Cardiomyocyte-specific PPARδ overexpression fully rescued the proliferation deficit observed in CD36-deficient neonatal hearts.
Cardiomyocyte-specific FABP5 reintroduction in adult mice was sufficient to trigger cell-cycle entry and resulted in significantly improved cardiac function following myocardial infarction.

Structured PICO

Does reintroducing FABP5 induce cardiomyocyte cell cycle entry and improve cardiac function following myocardial infarction in adult mice?

Population

Mice models including P1 WT, CD36KO, CD36CKO, PPARδCTG, and inducible CM-specific FABP5 knock-in (FABP5KI) mice, as well as isolated cardiomyocytes.

Intervention

Reintroduction of FABP5 in adult hearts using an inducible cardiomyocyte-specific FABP5 knock-in mouse (FABP5KI) following myocardial infarction.

Comparator

Control mice (implied, specific control group not explicitly detailed in abstract).

Outcome

Cardiomyocyte cell cycle entry and cardiac function following myocardial infarction.surrogate

Re-activating the RA/CD36/FABP5/PPARδ signaling pathway via FABP5 overexpression induces cardiomyocyte proliferation and functional recovery after ischemic injury in adult mice, highlighting a potential therapeutic target for cardiac regeneration.

Cite This Study

Salama et al. (2026) studied Myocardial infarction. FABP5 overexpression was evaluated on Cardiomyocyte cell cycle entry and cardiac function. Reintroducing FABP5 in adult mouse hearts drove cardiomyocyte cell cycle entry and significantly improved cardiac function following myocardial infarction.

synapsesocial.com/papers/6aae47640c69660b71ecc6d8 https://doi.org/10.1093/cvr/cvag206

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September 19, 2026Cardiovascular ResearchOpen Access

Reintroducing FABP5 in adult mice drives cardiomyocyte cell cycle entry and improves post-MI cardiac function.

View Full Paper

Ask AI

Bookmark

Why the study?

Does reintroducing FABP5 induce cardiomyocyte cell cycle entry and improve cardiac function following myocardial infarction in adult mice?

Population

Mice models including P1 WT, CD36KO, CD36CKO, PPARδCTG, and inducible CM-specific FABP5 knock-in mice, as…

Comparison

Reintroduction of FABP5 in adult hearts using an… vs Control mice.

Design

Preclinical

Key result

Reintroducing FABP5 in adult mouse hearts drove cardiomyocyte cell cycle entry and significantly improved cardiac function following myocardial infarction.

Authors

ASAbou Bakr M. Salama QOQinghui Ou MDMarc Dwenger

Discussion

Member takes

Overview

Should not yet alter post-MI care; leaves open whether FABP5 reactivation promotes human cardiomyocyte regeneration.

Key Points

To identify the molecular signaling pathway responsible for neonatal cardiomyocyte proliferation and determine whether reintroducing it into adult hearts can reactivate the cell cycle and promote cardiac regeneration.
Characterized neonatal hearts from wild-type, CD36-knockout (CD36KO), and conditional CD36-knockout (CD36cKO) postnatal day 1 mice using single-cell and bulk RNA sequencing, spatial transcriptomics, and metabolomics.
Assessed retinoic acid signaling in CD36KO and FABP5 knockdown cardiomyocytes, and evaluated in vivo rescue by crossing CD36KO with cardiomyocyte-specific PPARδ overexpression.
Engineered an inducible cardiomyocyte-specific FABP5 knock-in mouse model to assess cell-cycle activation and cardiac functional recovery following myocardial infarction in adult mice.
Identified a CD36/FABP5/PPARδ axis enriched in proliferating neonatal cardiomyocytes, with CD36 knockout leading to a 50% reduction in retinoic acid levels and abolishing retinoic acid-induced proliferation.
Cardiomyocyte-specific PPARδ overexpression fully rescued the proliferation deficit observed in CD36-deficient neonatal hearts.
Cardiomyocyte-specific FABP5 reintroduction in adult mice was sufficient to trigger cell-cycle entry and resulted in significantly improved cardiac function following myocardial infarction.

Structured PICO

Does reintroducing FABP5 induce cardiomyocyte cell cycle entry and improve cardiac function following myocardial infarction in adult mice?

Population

Mice models including P1 WT, CD36KO, CD36CKO, PPARδCTG, and inducible CM-specific FABP5 knock-in (FABP5KI) mice, as well as isolated cardiomyocytes.

Intervention

Reintroduction of FABP5 in adult hearts using an inducible cardiomyocyte-specific FABP5 knock-in mouse (FABP5KI) following myocardial infarction.

Comparator

Control mice (implied, specific control group not explicitly detailed in abstract).

Outcome

Cardiomyocyte cell cycle entry and cardiac function following myocardial infarction.surrogate

Cite This Study

synapsesocial.com/papers/6aae47640c69660b71ecc6d8 https://doi.org/10.1093/cvr/cvag206

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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