Evidence map›Paper›PMID 22535894›Full record

ReviewPhysiological reviews2012

Matricellular proteins in cardiac adaptation and disease.

Nikolaos G Frangogiannis

Open access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 247 papers.

0numbers the graph read from it
0cells of the map it votes in
247citing papers in PubMed
20.0field-weighted citation impact, top 1% of its field
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

247 citing papers in PubMed, 434 citations in OpenAlex.

  1. Article
  2. Decellularized cardiac ECM: A tissue-specific bioactive platform for drug release and cell delivery.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Review
  3. MMP12 induces fibrogenic macrophage differentiation to drive granuloma-associated cardiac fibrosis.American journal of respiratory and critical care medicine · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Osteopontin in Atrial Fibrillation and Atrial Remodeling.Journal of the American Heart Association · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Pericytes in tissue fibrosis.American journal of physiology. Cell physiology · 2025
    Review
  19. Article
  20. Review

187 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Nikolaos G FrangogiannisThe Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, 1300 Morris Park Ave., Forchheimer G46B, Bronx, NY 10461, USA. nikolaos.frangogiannis@einstein.yu.edu
Albert Einstein College of Medicine · US

Funding

Chemokines in Healing Myocardial InfarctsR01HL076246 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Nikolaos G Frangogiannis · 2005 to 2026
$9.5M
Resolution of Inflammation in healing Myocardial InfarctsR01HL085440 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2008 to 2025
$8.5M
NHLBI NIH HHS R01 HL076246NHLBI NIH HHS R01 HL085440NHLBI NIH HHS R01 HL-76246NHLBI NIH HHS R01 HL-85440
6 · The paper itself

Abstract

The term matricellular proteins describes a family of structurally unrelated extracellular macromolecules that, unlike structural matrix proteins, do not play a primary role in tissue architecture, but are induced following injury and modulate cell-cell and cell-matrix interactions. When released to the matrix, matricellular proteins associate with growth factors, cytokines, and other bioactive effectors and bind to cell surface receptors transducing signaling cascades. Matricellular proteins are upregulated in the injured and remodeling heart and play an important role in regulation of inflammatory, reparative, fibrotic and angiogenic pathways. Thrombospondin (TSP)-1, -2, and -4 as well as tenascin-C and -X secreted protein acidic and rich in cysteine (SPARC), osteopontin, periostin, and members of the CCN family (including CCN1 and CCN2/connective tissue growth factor) are involved in a variety of cardiac pathophysiological conditions, including myocardial infarction, cardiac hypertrophy and fibrosis, aging-associated myocardial remodeling, myocarditis, diabetic cardiomyopathy, and valvular disease. This review discusses the properties and characteristics of the matricellular proteins and presents our current knowledge on their role in cardiac adaptation and disease. Understanding the role of matricellular proteins in myocardial pathophysiology and identification of the functional domains responsible for their actions may lead to design of peptides with therapeutic potential for patients with heart disease.

Indexed as

Adaptation, PhysiologicalAgingAnimalsCCN Intercellular Signaling ProteinsExtracellular Matrix ProteinsFemaleHeartHeart DiseasesHumansMaleMiceOsteopontinRatsTenascinThrombospondinsVentricular RemodelingCCN Intercellular Signaling ProteinsExtracellular Matrix ProteinsOsteopontinTenascinThrombospondins

Identifiers

PMID22535894
PMCPMC4411042
OpenAlexW2068569386

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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 OpenQuestion graph.