Evidence map›Paper›PMID 31566432›Full record

ReviewAmerican journal of physiology. Renal physiology2019

Macrophage polarization in chronic kidney disease: a balancing act between renal recovery and decline?

Jason E Engel, Alejandro R Chade

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. GPR183 contributes to renal macrophage infiltration and fibrosis in kidney injury.American journal of physiology. Renal physiology · 2026
    Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Observational
  17. CX3CR1 regulates the development of renal interstitial fibrosis through macrophage polarization.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  18. Review
  19. Macrophages-Stealth Cells Below the Radar.Kidney international reports · 2023
    Article
  20. Article
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

2 authors at 1 institution in 1 country.

Jason E EngelDepartment of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi.
Alejandro R ChadeDepartment of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi.
Jackson Memorial Hospital · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HALL, JOHN E · 1993 to 2018
$39.4M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
Microcirculation in Renovascular HypertensionR01HL095638 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI CHADE, ALEJANDRO ROBERTO · 2010 to 2021
$3.9M
NHLBI NIH HHS P01 HL051971NHLBI NIH HHS R01 HL095638NIGMS NIH HHS P20 GM104357
6 · The paper itself

Abstract

Macrophages are heterogenous cells of the innate immune system that can fluidly modulate their phenotype to respond to their local microenvironment. They are found throughout the renal compartments, where they contribute to homeostasis and function. However, renal injury activates molecular pathways that initially stimulate differentiation of macrophages into a proinflammatory M1 phenotype. Later in the course of healing, abundant apoptotic debris and anti-inflammatory cytokines induce the production of anti-inflammatory M2 macrophages, which contribute to tissue regeneration and repair. Thus, the dynamic balance of M1 and M2 populations may outline the burden of inflammation and process of tissue repair that define renal outcomes, which has been the impetus for therapeutic efforts targeting macrophages. This review will discuss the role of these phenotypes in the progression of chronic renal injury, potential pathogenic mechanisms, and the promise of macrophage-based therapeutic applications for chronic kidney disease.

Indexed as

AnimalsCell PolarityDisease ProgressionHumansMacrophage ActivationMacrophagesRecovery of FunctionRenal Insufficiency, Chronicchronic kidney diseasefibrosisinflammationmacrophagestissue repair

Identifiers

PMID31566432
PMCPMC6962510
OpenAlexW2979006802

What OpenQuestion holds

Textmetadata
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.