Target intelligence / Profile preview

Cardiac remodeling pathways

Molecular classification
Transcription factor (e.g., NF-κB, Nrf2), Enzyme (e.g., matrix metalloproteinases), Receptor (e.g., angiotensin II receptor, TGF-β receptor), Kinase (e.g., PI3K, MAPK, JAK/STAT), Cytokine/Growth factor (e.g., TGF-β, TNF-α), Other (signal transduction networks, microRNAs, etc.)
01

Overview

Cardiac remodeling pathways comprise a complex network of molecular and cellular signaling mechanisms that drive structural and functional changes in the heart, particularly after injury (such as myocardial infarction), chronic pressure, or volume overload. These processes involve myocyte death, hypertrophy, fibrosis, inflammation, extracellular matrix remodeling, angiogenesis, and altered metabolic activity. Pathological remodeling is central in the progression to heart failure and has become a major focus for therapeutic intervention, with multiple drug classes targeting specific aspects of these cascades. However, “cardiac remodeling pathways” is not a single molecule or receptor, but rather a collective term for multiple interlinked targets and mechanisms involved in adverse or adaptive cardiac remodeling.

Other names
Cardiac remodeling signaling pathwaysMyocardial remodeling pathwaysVentricular remodeling pathwaysHeart remodeling mechanisms
02

Mechanism of action

Inhibition of neurohormonal signaling (e.g., angiotensin II, sympathetic activation) Anti-fibrotic action (such as TGF-β pathway inhibition) Inhibition of matrix metalloproteinases (reducing extracellular matrix remodeling) Modulation of inflammation (e.g., NF-κB inhibition) Reduction of cellular hypertrophy and apoptosis Enhancing autophagy and metabolic regulation

03

Biological functions

Signal transductionCell death (apoptosis, necrosis, autophagy)InflammationCell proliferation and hypertrophyFibrosis/extracellular matrix remodelingAngiogenesisMetabolic regulation
04

Disease associations

Cardiovascular disease (especially heart failure, myocardial infarction, cardiomyopathy, and post-injury states)InflammationOther (secondary involvement in hypertension, metabolic syndrome, etc.)
05

Safety considerations

Off-target effects due to broad pathway modulation (e.g., immune suppression, renal dysfunction, electrolyte disturbances)Hypotension, bradycardia (with beta-blockers, ACE inhibitors)Hyperkalemia (with mineralocorticoid antagonists)Unforeseen adverse effects in targeting complex biological networks
06

Interacting drugs

Beta-blockers (e.g., carvedilol, metoprolol)

6 more in the full profile.

07

Biomarkers

Natriuretic peptides (BNP, NT-proBNP)Cardiac troponinsGalectin-3Soluble ST2Markers of ECM turnover (e.g., MMPs, TIMPs)

Beyond the preview

Go deeper on Cardiac remodeling pathways.

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Cardiac remodeling pathways.

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call