Evidence mapPaperPMID 40908522Full record

ReviewCardiovascular & hematological disorders drug targets2026

Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.

Ankita Wal, Anurag Rawat, Rakesh Verma, Azhar Rasheed, Uttam Prasad Panigrahy, Anwesha Das, Amin Gasmi

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In one paragraph

Review in Cardiovascular & hematological disorders drug targets, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Ankita WalDepartment of Pharmacy, PSIT-Pranveer Singh of Institute of Technology (Pharmacy), NH19 Kanpur Agra highway Bhauti Kanpur, Kanpur, India.
Anurag RawatCardiology, Himalayan Institute of Medical Science, Dehradun, India.
Rakesh VermaDepartment of Pharmacology, Institute of Medical Science, BHU, Varanasi, India.
Azhar RasheedDepartment of Pharmacy, PSIT-Pranveer Singh of Insitute of technology (Pharmacy), NH19 Kanpur Agra highway Bhauti Kanpur, Kanpur, India.
Uttam Prasad PanigrahyFaculty of Pharmaceutical Science, Assam Down Town University, Sankar, Madhab Path, GandhiNagar, Panikhaiti, Guwahati, Assam, India.
Anwesha DasSanaka Educational Trust's Group of Institutions, Malandighi P.S. Kanksha, Durgapur, West Bengal, India.
Amin GasmiSociété Francophone de Nutrithérapie et de NutrigénétiqueAppliquée, Villeurbanne, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCardiovascular disorders (CVDs) remain the leading cause of global mortality, surpassing other chronic illnesses. An alarming rise in CVD-related deaths, particularly among younger populations, has intensified research efforts to better understand the disease and its complications. Among these, myocardial fibrosis plays a central role in the development of cardiac dysfunction and heart failure. Given its multifactorial nature, diverse therapeutic strategies are required to manage its progression effectively.

methodsA comprehensive literature review was conducted using databases such as PubMed, Scopus, Elsevier, and ClinicalTrials.gov. Only peer-reviewed, English-language studies focusing on molecular mechanisms and therapeutic strategies for myocardial fibrosis were included. Irrelevant, non-English, and non-peer-reviewed sources were excluded. Data from selected preclinical and clinical investigations were qualitatively synthesized.

resultsMyocardial fibrosis arises from various pathological conditions, including ischemia, hyperlipidemia, and genetic disorders, which promote maladaptive cardiac remodeling. Although traditional treatments such as RAAS inhibitors and β-blockers offer symptomatic relief, they do not halt disease progression. Recent evidence suggests that multiple molecular pathways are involved in the development of fibrosis, opening opportunities to explore alternative therapeutic targets. DISCUSSION: Due to its complex pathophysiology, myocardial fibrosis cannot be addressed by monotherapy alone. Anti-TGF-β agents have emerged as promising candidates, alongside newer therapies like SGLT2 inhibitors and MMP inhibitors. Additionally, regenerative approaches, such as stem cell and gene therapy, offer future avenues, though technical and safety challenges accompany them.

conclusionMyocardial fibrosis remains a critical contributor to heart failure, and current treatments are insufficient to reverse its course. A multifaceted therapeutic approach targeting different molecular mechanisms holds the key to improved clinical outcomes. Continued translational research is crucial for advancing emerging therapies from bench to bedside.

Indexed as

CardiomyopathiesCardiovascular DiseasesMyocardiumAnimalsFibrosisHumansMolecular Targeted Therapymatrix metalloproteinasesmyocardial fibrosisRAAS inhibitorsSGLT2 inhibitorsTGF-β inhibitor

Identifiers

What Socratic holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.