Evidence map›Paper›PMID 25795504›Full record

ReviewSeminars in nephrology2015

Mitochondrial function and disturbances in the septic kidney.

Samir M Parikh, Yuan Yang, Liyu He, Chengyuan Tang, Ming Zhan, Zheng Dong

Abstract readReview
In one paragraph

Review in Seminars in nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 1 pooled it
–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

106 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Observational
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

46 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

6 authors.

Samir M ParikhDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA. Electronic address: sparikh1@bidmc.harvard.edu.
Yuan YangDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Liyu HeDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Chengyuan TangDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Ming ZhanDepartment of Pathology and Medicine, Northwestern University, Chicago, IL.
Zheng DongDepartment of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Cellular Biology and Anatomy, Georgia Regents University and Charlie Norwood VA Medical Center, Augusta, GA.

Funding

Mitochondrial Biogenesis in Kidney DiseaseR01DK095072 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Samir M Parikh · 2012 to 2026
$5.3M
NIDDK NIH HHS R01 DK095072
6 · The paper itself

Abstract

Per milligram of tissue, only the heart exceeds the kidney's abundance of mitochondria. Not surprisingly, renal mitochondria are most densely concentrated in the epithelium of the nephron, at sites where the chemical work of moving solutes against electrochemical gradients places large and constant demands for adenosine triphosphate. Derangements of renal epithelial mitochondria appear to be a hallmark for diverse forms of acute kidney injury (AKI). The pathogenesis of multiple-organ dysfunction syndrome in sepsis is complex, but a substantial body of experimental and observational human data supports the twin concepts that mitochondrial dysfunction contributes to impaired filtration and that recovery of mitochondrial structure and function is essential for recovery from sepsis-associated AKI. These insights have suggested novel methods to diagnose, stratify, prevent, or even treat this common and deadly complication of critical illness. This review will do the following: (1) describe the structure and functions of healthy mitochondria and how renal energy metabolism relates to solute transport; (2) provide an overview of the evidence linking mitochondrial pathology to renal disease; (3) summarize the mitochondrial lesions observed in septic AKI; (4) analyze the role of mitochondrial processes including fission/fusion, mitophagy, and biogenesis in the development of septic AKI and recovery from this disease; and (5) explore the potential for therapeutically targeting mitochondria to prevent or treat septic AKI.

Indexed as

Acute Kidney InjuryEnergy MetabolismEpithelial CellsHumansKidneyMitochondriaMitochondrial DynamicsMitophagyOrganelle BiogenesisSepsiskidney injurymitochondriaSepsis

Identifiers

PMID25795504
PMCPMC4465453

What OpenQuestion holds

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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 OpenQuestion graph.