GO:0010665 regulation of cardiac muscle cell apoptotic process: Apoptosis Control, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0010665 describes any process that modulates the rate or extent of cardiac muscle cell apoptosis, a caspase-dependent form of programmed cell death.
• The term is a biological_process node that sits at the intersection of cardiomyocyte survival signaling, mitochondrial homeostasis, and ischemia-reperfusion injury.
• Key regulators include SIRT1, HIF-1α/BNIP3, ADAR2, AVEN, RBFox1, Nrf2, Septin4, and acid sphingomyelinase, each acting on distinct pro- or anti-apoptotic arms.
• Dysregulation of this process is central to myocardial infarction, heart failure, doxorubicin cardiotoxicity, and diabetic cardiomyopathy.
• CRISPR knockout, point-mutation, knock-in, and overexpression models allow causal dissection of each regulator in primary cardiomyocytes or iPSC-derived cardiac cells.
• GO:0010665 is best studied with combined readouts: caspase-3/7 activity, TUNEL, mitochondrial membrane potential, and transcriptomic or proteomic profiling.
Description
GO:0010665, regulation of cardiac muscle cell apoptotic process, is a Gene Ontology biological_process term that captures any molecular event modulating the rate or extent of programmed death of cardiac muscle cells. Cardiac muscle cells, or cardiomyocytes, are terminally differentiated and largely non-proliferative, so their loss through apoptosis directly reduces contractile capacity and drives adverse remodeling. The term therefore describes a regulatory hub rather than a single pathway: it includes transcriptional, post-transcriptional, and mitochondrial control points that either promote or suppress caspase activation in the heart. Mechanistically, regulation of cardiac muscle cell apoptosis is executed through the intrinsic mitochondrial pathway, in which BH3-only proteins and Bcl-2 family members govern cytochrome c release and apoptosome formation. Extrinsic signals from oxidative stress, calcium overload, and inflammatory cytokines feed into this core machinery, while survival kinases and deacetylases buffer the response. Because the same regulators are frequently altered in human cardiovascular disease, GO:0010665 is a high-value annotation for translational cardiology. For researchers, GO:0010665 provides a standardized vocabulary to connect genotype to phenotype: a gene annotated to this term is expected to change cardiomyocyte viability under stress, and CRISPR-based perturbation is the most direct way to test that expectation. This article summarizes the definition, core mechanisms, key genes, disease links, and experimental methods relevant to GO:0010665, with all factual claims tied to published literature.
regulation of cardiac muscle cell apoptotic process At A Glance
| GO ID | GO:0010665 |
|---|---|
| GO term | regulation of cardiac muscle cell apoptotic process |
| Ontology | biological_process |
| Synonym | regulation of cardiac muscle cell apoptosis |
| Definition | Any process that modulates the rate or extent of cardiac cell apoptotic process, a form of programmed cell death induced by external or internal signals that trigger the activity of proteolytic caspases whose actions dismantle a cardiac muscle cell and result in its death. |
| Major function | Controls cardiomyocyte survival versus caspase-dependent death under stress such as ischemia-reperfusion, oxidative injury, and cardiotoxic drugs. |
| Key upstream regulators | SIRT1, HIF-1α/BNIP3, ADAR2, AVEN, RBFox1, Nrf2, Septin4, acid sphingomyelinase. |
| Disease relevance | Myocardial infarction, heart failure, doxorubicin cardiotoxicity, diabetic cardiomyopathy. |
| Experimental readouts | Caspase-3/7 activity, TUNEL, mitochondrial membrane potential, infarct size, echocardiography. |
What Is GO:0010665?
In plain terms, GO:0010665 describes the set of processes that dial the rate of cardiac muscle cell suicide up or down. Formally, it is any process that modulates the rate or extent of cardiac cell apoptotic process, a form of programmed cell death induced by external or internal signals that trigger the activity of proteolytic caspases whose actions dismantle a cardiac muscle cell and result in its death. The term is a regulation node: it does not itself execute apoptosis but controls the upstream signals, mitochondrial checkpoints, and caspase activation that determine whether a cardiomyocyte survives or dies.
Why Is regulation of cardiac muscle cell apoptotic process Important in Cell Biology?
GO:0010665 matters because cardiomyocyte apoptosis is a final common pathway of cardiac injury, and its regulation determines whether the heart compensates or fails after ischemia, pressure overload, or chemotherapy. Unlike proliferating tissues, the heart cannot readily replace lost cardiomyocytes, so even modest shifts in the apoptotic threshold have outsized functional consequences. Annotating genes to GO:0010665 therefore helps prioritize therapeutic targets and interpret omics data in cardiovascular research.
• Cardiomyocytes are terminally differentiated, so apoptosis directly translates into irreversible loss of contractile units.
• Ischemia-reperfusion injury activates both autophagy and apoptosis, and the balance is regulated by SIRT1 and HIF-1α/BNIP3.
• Doxorubicin cardiotoxicity is limited by anti-apoptotic regulators such as ADAR2 and Nrf2.
• AVEN acts as an apoptotic repressor whose downregulation exacerbates cardiac injury after myocardial infarction.
• RBFox1 is cardioprotective in myocardial infarction-induced heart failure, linking RNA processing to apoptosis control.
• Acid sphingomyelinase promotes diabetic cardiomyopathy by disrupting mitochondrial calcium homeostasis and apoptosis.
• Septin4 regulates cardiac fibrosis after pressure overload, connecting apoptosis regulation to fibrotic remodeling.
• GO:0010665 provides a shared vocabulary for comparing cardioprotective interventions across model systems.
• CRISPR perturbation of annotated genes enables causal testing of survival versus death phenotypes.
• The term supports drug discovery by defining which molecular nodes can be targeted to reduce cardiomyocyte death.
What Happens During regulation of cardiac muscle cell apoptotic process?
Initiation by stress signals
In simple terms: The process starts when the heart cell receives a danger signal such as low oxygen, oxidative stress, or a toxic drug.
Regulation of cardiac muscle cell apoptosis begins with external or internal signals that include ischemia-reperfusion, reactive oxygen species, calcium overload, and chemotherapeutic exposure. These signals activate stress-responsive transcription factors and kinases that set the apoptotic threshold, such as HIF-1α and Nrf2. In ischemia-reperfusion, SIRT1 modulates autophagy and survival signaling, thereby influencing whether cardiomyocytes commit to death. Acid sphingomyelinase activity during diabetic cardiomyopathy disrupts mitochondrial calcium homeostasis and initiates pro-apoptotic signaling.
Mitochondrial checkpoint and Bcl-2 family control
In simple terms: The mitochondria act as a switchboard that decides whether the cell will die.
The intrinsic apoptotic pathway is controlled at the mitochondrial outer membrane by Bcl-2 family proteins, and BNIP3 is a key BH3-only effector downstream of HIF-1α in cardiomyocytes. HIF-1α/BNIP3 signaling-induced autophagy plays a protective role during myocardial ischemia-reperfusion injury, indicating that mitochondrial quality control is coupled to apoptosis regulation. Acid sphingomyelinase promotes diabetic cardiomyopathy via disruption of mitochondrial calcium homeostasis, which sensitizes mitochondria to permeability transition and death signaling. AVEN functions as an apoptotic repressor, and its downregulation exacerbates cardiac injury after myocardial infarction, placing it at the mitochondrial checkpoint.
Caspase activation and dismantling
In simple terms: Once the decision is made, executioner enzymes chop up the cell.
The QuickGO definition specifies that apoptosis is triggered by proteolytic caspases whose actions dismantle a cardiac muscle cell and result in its death. In experimental cardiology, caspase-3/7 activity and TUNEL staining are standard readouts of this execution phase. Regulators annotated to GO:0010665 act upstream of or at the level of caspase activation, determining whether the proteolytic cascade is engaged. Because caspases are the terminal effectors, interventions that preserve mitochondrial integrity or raise the apoptotic threshold reduce caspase activation and cardiomyocyte loss.
Resolution, remodeling, and fibrosis
In simple terms: After cells die, the heart tries to repair itself, often with scar tissue.
Loss of cardiomyocytes through apoptosis triggers compensatory remodeling, including fibrosis and hypertrophy, which are themselves regulated processes. Septin4 regulates cardiac fibrosis after pressure overload, linking the apoptotic response to fibrotic gene programs. RBFox1 is cardioprotective in myocardial infarction-induced heart failure, suggesting that RNA-binding proteins shape the transition from acute apoptosis to chronic failure. ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity, indicating that beneficial remodeling pathways can be harnessed to limit apoptosis.
Pharmacological and exercise modulation
In simple terms: Drugs and exercise can push the system toward survival.
Tanshinone I inhibits doxorubicin-induced cardiotoxicity by regulating the Nrf2 signaling pathway, demonstrating that pharmacological activation of antioxidant programs can suppress cardiomyocyte apoptosis. ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity, providing a molecular link between exercise and apoptosis regulation. SIRT1 is a regulator of autophagy with implications for the progression and treatment of myocardial ischemia-reperfusion, highlighting deacetylase-dependent control of survival. These examples show that GO:0010665 is a druggable and lifestyle-modifiable node.
Key Genes Involved in GO:0010665 regulation of cardiac muscle cell apoptotic process
The following genes and proteins have been experimentally linked to regulation of cardiac muscle cell apoptotic process (GO:0010665) in the cited literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| SIRT1 | Regulates autophagy and survival signaling during myocardial ischemia-reperfusion | Target for cardioprotection and autophagy-apoptosis crosstalk studies |
| HIF-1α | Stress-responsive transcription factor upstream of BNIP3 | Hypoxia signaling node in ischemia-reperfusion injury |
| BNIP3 | BH3-only effector mediating autophagy and mitochondrial control | Mitochondrial checkpoint in cardiomyocyte death |
| Septin4 | Regulates cardiac fibrosis after pressure overload | Links apoptosis regulation to fibrotic remodeling |
| Nrf2 | Antioxidant transcription factor suppressed by doxorubicin toxicity | Pharmacological target for cardiotoxicity prevention |
| ADAR2 | RNA editing enzyme increased in exercised heart; protects against infarction and doxorubicin toxicity | Exercise mimetic and cardioprotective mediator |
| Acid sphingomyelinase | Promotes diabetic cardiomyopathy via mitochondrial calcium disruption | Sphingolipid-mitochondria axis in diabetic heart |
| RBFox1 | Cardioprotective RNA-binding protein in infarction-induced heart failure | RNA processing regulator of apoptosis and failure |
| AVEN | Apoptotic repressor; downregulation exacerbates cardiac injury after infarction | Anti-apoptotic checkpoint in myocardial infarction |
| Caspase-3 | Executioner protease in apoptosis | Terminal readout of apoptotic commitment |
| Caspase-7 | Executioner protease in apoptosis | Terminal readout of apoptotic commitment |
| Bcl-2 family members | Govern mitochondrial outer membrane permeabilization | Checkpoint proteins for survival-death decisions |
| Cytochrome c | Released from mitochondria during intrinsic apoptosis | Marker of mitochondrial apoptosis commitment |
| Calcium channels (mitochondrial) | Maintain mitochondrial calcium homeostasis | Target in diabetic cardiomyopathy |
| Autophagy machinery | Interacts with apoptosis regulation during ischemia-reperfusion | Crosstalk node for survival versus death |
| RNA editing machinery | ADAR2-dependent editing protects the heart | Post-transcriptional layer of apoptosis control |
| Fibrosis gene programs | Activated after cardiomyocyte loss | Remodeling outcome of apoptotic injury |
How Is regulation of cardiac muscle cell apoptotic process Regulated?
Regulation of cardiac muscle cell apoptotic process is controlled at multiple levels. SIRT1 modulates autophagy and survival signaling during myocardial ischemia-reperfusion, coupling deacetylation to apoptotic threshold. HIF-1α/BNIP3 signaling-induced autophagy plays a protective role during myocardial ischemia-reperfusion injury, showing that hypoxia-responsive transcription and mitochondrial autophagy intersect with apoptosis regulation. Nrf2 signaling mediates the protective effect of Tanshinone I against doxorubicin-induced cardiotoxicity, indicating redox-sensitive transcriptional control. ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity, adding an RNA-editing layer. Acid sphingomyelinase activity disrupts mitochondrial calcium homeostasis in diabetic cardiomyopathy, providing a lipid-enzyme regulatory input. AVEN acts as an apoptotic repressor whose downregulation exacerbates cardiac injury after myocardial infarction, and RBFox1 is cardioprotective in infarction-induced heart failure, together illustrating post-transcriptional and RNA-binding control.
regulation of cardiac muscle cell apoptotic process and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| SIRT1 | Myocardial ischemia-reperfusion injury | Cardiomyocyte-specific knockout and overexpression in ischemia-reperfusion models |
| HIF-1α / BNIP3 | Ischemia-reperfusion injury and hypoxia response | Hypoxia-reoxygenation in primary cardiomyocytes with pathway perturbation |
| Nrf2 | Doxorubicin-induced cardiotoxicity | Doxorubicin-treated cardiomyocytes with Nrf2 pathway modulation |
| ADAR2 | Myocardial infarction and doxorubicin cardiotoxicity | Exercise-mimetic and ADAR2 gain-of-function models |
| Acid sphingomyelinase | Diabetic cardiomyopathy | Diabetic mouse models with sphingomyelinase inhibition |
| AVEN | Cardiac injury after myocardial infarction | AVEN knockdown and rescue in infarction models |
| RBFox1 | Infarction-induced heart failure | RBFox1 overexpression and loss-of-function in heart failure models |
| Septin4 | Cardiac fibrosis after pressure overload | Pressure-overload models with Septin4 perturbation |
Myocardial infarction and ischemia-reperfusion injury
Myocardial infarction and subsequent reperfusion are classic triggers of cardiomyocyte apoptosis, and regulators annotated to GO:0010665 determine infarct size and functional recovery. SIRT1 is a regulator of autophagy with implications for the progression and treatment of myocardial ischemia-reperfusion, making it a candidate therapeutic node. HIF-1α/BNIP3 signaling-induced autophagy plays a protective role during myocardial ischemia-reperfusion injury, indicating that hypoxia-driven autophagy can limit apoptotic death. AVEN downregulation exacerbates cardiac injury after myocardial infarction, confirming that endogenous apoptotic repressors are required for tissue preservation. RBFox1 is cardioprotective in myocardial infarction-induced heart failure, linking RNA processing to long-term outcomes.
Doxorubicin cardiotoxicity
Doxorubicin is a widely used chemotherapeutic whose clinical use is limited by cardiomyocyte apoptosis. Tanshinone I inhibits doxorubicin-induced cardiotoxicity by regulating the Nrf2 signaling pathway, demonstrating that antioxidant transcriptional programs can suppress apoptosis. ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity, suggesting that RNA editing contributes to cardioprotection. These studies position GO:0010665 as a mechanistic framework for developing cardioprotective adjuvants during cancer therapy.
Diabetic cardiomyopathy
Diabetic cardiomyopathy involves metabolic and calcium-handling disturbances that converge on cardiomyocyte apoptosis. Acid sphingomyelinase promotes diabetic cardiomyopathy via disruption of mitochondrial calcium homeostasis, directly connecting sphingolipid metabolism to apoptotic regulation. Because mitochondrial calcium overload sensitizes cardiomyocytes to death, regulators annotated to GO:0010665 are plausible targets for preserving cardiac function in diabetes.
Pressure overload, fibrosis, and heart failure
Chronic pressure overload and post-infarction remodeling involve ongoing cardiomyocyte loss and fibrosis, processes regulated in part through GO:0010665. Septin4 regulates cardiac fibrosis after pressure overload, linking apoptotic regulation to extracellular matrix deposition. RBFox1 is cardioprotective in myocardial infarction-induced heart failure, indicating that RNA-binding proteins can modify the transition from acute injury to chronic failure. Together, these findings show that regulation of cardiac muscle cell apoptosis shapes both acute and chronic cardiac disease phenotypes.
From regulation of cardiac muscle cell apoptotic process-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for cardiomyocyte survival? | CRISPR knockout in cardiomyocytes or iPSC-derived cardiac cells |
| Does a specific amino acid change alter anti-apoptotic activity? | CRISPR point mutation knock-in at the endogenous locus |
| Does a disease-associated variant change apoptotic threshold? | Knock-in of the variant with isogenic controls |
| Where and when is the protein expressed during injury? | Tagged knock-in with fluorescent or epitope tag |
| Does increased dosage protect against apoptosis? | CRISPR overexpression or cDNA overexpression |
| Which pathways cooperate with the candidate gene? | CRISPR library screening combined with apoptosis readouts |
How to Study the regulation of cardiac muscle cell apoptotic process Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Caspase-3/7 activity assay | Executioner caspase activity | Quantifying apoptotic commitment after stress |
| TUNEL staining | DNA fragmentation in apoptotic nuclei | Histological assessment of cardiomyocyte death |
| Annexin V flow cytometry | Phosphatidylserine externalization | Early apoptosis detection in cultured cardiomyocytes |
| Mitochondrial membrane potential imaging | Mitochondrial integrity | Assessing intrinsic pathway activation |
| RNA sequencing | Transcriptome changes | Identifying regulators and GO enrichment |
| Proteomics | Protein abundance and modifications | Discovering post-transcriptional regulators |
| Echocardiography | Cardiac function in vivo | Linking molecular regulation to organ phenotype |
| Histology for fibrosis | Extracellular matrix deposition | Assessing remodeling after apoptotic injury |
Apoptosis phenotyping assays
Caspase-3/7 activity, TUNEL staining, annexin V flow cytometry, and mitochondrial membrane potential measurements are standard methods to quantify regulation of cardiac muscle cell apoptosis. These readouts are used in ischemia-reperfusion, doxorubicin, and diabetic cardiomyopathy models to determine whether a perturbation shifts the apoptotic threshold. Combining multiple assays reduces the risk of confounding necrosis with apoptosis.
Transcriptomic and proteomic profiling
RNA sequencing and proteomics can identify genes and proteins whose expression changes in parallel with apoptotic commitment, helping annotate candidates to GO:0010665. In myocardial infarction and heart failure models, such profiling has implicated RNA-binding proteins and editing enzymes in cardioprotection. Pathway enrichment against Gene Ontology terms, including GO:0010665, provides a structured interpretation of omics data.
Mitochondrial and calcium imaging
Live-cell imaging of mitochondrial membrane potential, calcium transients, and reactive oxygen species reveals the upstream events that regulate apoptosis in cardiomyocytes. Acid sphingomyelinase disruption of mitochondrial calcium homeostasis in diabetic cardiomyopathy illustrates how imaging can pinpoint the regulatory step. HIF-1α/BNIP3-dependent autophagy during ischemia-reperfusion similarly requires mitochondrial readouts to distinguish protective from detrimental responses.
In vivo cardiac function and histology
Echocardiography, infarct size measurement, and histological assessment of fibrosis are used to connect molecular regulation of apoptosis to organ-level outcomes. Septin4 regulation of cardiac fibrosis after pressure overload was demonstrated with such in vivo approaches. AVEN downregulation exacerbating cardiac injury after myocardial infarction and RBFox1 cardioprotection in heart failure were likewise validated in animal models.
How CRISPR Can Be Used to Study GO:0010665 regulation of cardiac muscle cell apoptotic process
Knockout
CRISPR knockout of a candidate gene is the most direct way to test whether it is required for regulation of cardiac muscle cell apoptosis. Loss-of-function studies of AVEN and RBFox1 demonstrated exacerbated cardiac injury and loss of cardioprotection, respectively, establishing causal roles. Knockout models can be combined with ischemia-reperfusion, doxorubicin, or diabetic stressors to reveal context-dependent effects.
Point Mutation
CRISPR point mutation knock-in allows testing of specific residues or disease-associated variants without altering gene dosage. This is valuable for regulators such as ADAR2 or AVEN where catalytic or interaction domains can be dissected. Point-mutant models help distinguish loss-of-function from dominant-negative or gain-of-function mechanisms in apoptosis regulation.
Knock-in
Knock-in of reporters, tags, or human disease variants provides spatial and temporal resolution of gene function in the heart. Tagged knock-in of Septin4 or RBFox1 enables tracking of protein localization during pressure overload or infarction. Disease-variant knock-in with isogenic controls is a rigorous approach to link genotype to apoptotic phenotype.
Overexpression
CRISPR activation or cDNA overexpression tests whether increased dosage of a regulator is sufficient to protect cardiomyocytes from apoptosis. ADAR2 gain-of-function is cardioprotective against infarction and doxorubicin toxicity, illustrating the value of overexpression models. Nrf2 pathway activation by Tanshinone I similarly shows that boosting a survival program reduces cardiotoxicity.
How EDITGENE Supports regulation of cardiac muscle cell apoptotic process Research
Researchers studying regulation of cardiac muscle cell apoptotic process-related genes often need to determine whether a candidate gene is causally involved in cardiomyocyte survival or death, and CRISPR-based perturbation is the most direct route to that answer. EDITGENE provides end-to-end cell model generation and screening services tailored to cardiovascular apoptosis research.
Contact EDITGENE today to design your custom CRISPR model for regulation of cardiac muscle cell apoptotic process research.
Frequently Asked Questions About regulation of cardiac muscle cell apoptotic process
What is GO:0010665 regulation of cardiac muscle cell apoptotic process?
GO:0010665 is a Gene Ontology biological_process term defined as any process that modulates the rate or extent of cardiac cell apoptotic process, a caspase-dependent form of programmed cell death in cardiac muscle cells.
What genes are involved in regulation of cardiac muscle cell apoptotic process?
Reported regulators include SIRT1, HIF-1α, BNIP3, Septin4, Nrf2, ADAR2, acid sphingomyelinase, RBFox1, and AVEN.
How is cardiac muscle cell apoptosis regulated during ischemia-reperfusion?
SIRT1 modulates autophagy and survival signaling, while HIF-1α/BNIP3-induced autophagy plays a protective role during myocardial ischemia-reperfusion injury.
Which pathways protect cardiomyocytes from doxorubicin-induced apoptosis?
Nrf2 signaling mediates protection by Tanshinone I, and ADAR2 protects against doxorubicin-induced cardiotoxicity.
What is the role of AVEN in cardiac apoptosis?
AVEN is an apoptotic repressor, and its downregulation exacerbates cardiac injury after myocardial infarction.
How does acid sphingomyelinase contribute to diabetic cardiomyopathy?
Acid sphingomyelinase promotes diabetic cardiomyopathy via disruption of mitochondrial calcium homeostasis, sensitizing cardiomyocytes to apoptosis.
What methods are used to study regulation of cardiac muscle cell apoptosis?
Common methods include caspase-3/7 activity assays, TUNEL, annexin V flow cytometry, mitochondrial membrane potential imaging, RNA sequencing, proteomics, and echocardiography.
Can CRISPR be used to study GO:0010665?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models allow causal testing of candidate regulators in cardiomyocytes and iPSC-derived cardiac cells.
What is the role of RBFox1 in heart failure?
RBFox1 is cardioprotective in myocardial infarction-induced heart failure, linking RNA processing to apoptosis regulation.
How does Septin4 relate to cardiac fibrosis?
Septin4 regulates cardiac fibrosis after pressure overload, connecting apoptotic regulation to fibrotic remodeling.
Conclusion
GO:0010665, regulation of cardiac muscle cell apoptotic process, is a central biological_process term for understanding how cardiomyocytes decide between survival and caspase-dependent death. The cited literature identifies SIRT1, HIF-1α/BNIP3, Nrf2, ADAR2, acid sphingomyelinase, RBFox1, AVEN, and Septin4 as key regulators operating across transcriptional, post-transcriptional, mitochondrial, and lipid signaling layers. These regulators are directly relevant to myocardial infarction, heart failure, doxorubicin cardiotoxicity, and diabetic cardiomyopathy. For researchers, CRISPR-based knockout, point mutation, knock-in, overexpression, and library screening provide the causal toolkit needed to move from annotation to mechanism. Combining these perturbations with apoptosis phenotyping, omics, and in vivo cardiac function readouts will continue to refine the regulatory map of GO:0010665 and support therapeutic target discovery.
References
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- 2. Zhang Y et al.. 2019. HIF-1α/BNIP3 signaling pathway-induced-autophagy plays protective role during myocardial ischemia-reperfusion injury.. Biomed Pharmacother 120:109464 PMID: 31590128
- 3. Yücel D et al.. 2025. Septin4 Regulates Cardiac Fibrosis After Pressure Overload.. Circ Res 137(8):1117-1132 PMID: 40960950
- 4. Jiang Q et al.. 2022. Tanshinone I inhibits doxorubicin-induced cardiotoxicity by regulating Nrf2 signaling pathway.. Phytomedicine 106:154439 PMID: 36108374
- 5. Wu X et al.. 2022. ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity.. Mol Ther 30(1):400-414 PMID: 34274534
- 6. Wei Y et al.. 2025. Acid sphingomyelinase promotes diabetic cardiomyopathy via disruption of mitochondrial calcium homeostasis.. Cardiovasc Diabetol 24(1):272 PMID: 40640752
- 7. He M et al.. 2025. Cardioprotective role of RBFox1 in myocardial infarction-induced heart failure.. Cardiovasc Res 121(16):2534-2548 PMID: 41294183
- 8. Yu P et al.. 2023. Downregulation of apoptotic repressor AVEN exacerbates cardiac injury after myocardial infarction.. Proc Natl Acad Sci U S A 120(42):e2302482120 PMID: 37816050
