Inflammatory cells in renal regeneration

被引:20
作者
Ghielli, M
Verstrepen, WA
Nouwen, EJ
DeBroe, ME
机构
关键词
D O I
10.3109/08860229609052806
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Much research has been performed to gain better insight into the regeneration process, responsible for the functional and morphological recovery after acute renal failure (ARF). Many investigators focused on endogenously produced polypeptide growth factors as the major mediators of tubular epithelial cell proliferation. However arguments contradicting this hypothesis have recently gained more support. Indeed, the early decrease of renal epidermal growth factor (EGF) and insulinlike growth factor-1 (IGF-1) in different experimental models of ARF has been frequently shown at both the mRNA and protein level, while other growth factors could not be shown to increase. Moreover the inaccessibility of the upregulated receptors for endogenously produced growth factors has encouraged research to seek alternative origins for the signals inducing renal regeneration. The accumulation of mononuclear leukocytes in the renal interstitium is a striking observation in renal failure. Where the interstitial disease, recognized by the persistent interstitial accumulation of leukocytes, is a better predictor of chronic renal failure and developing fibrosis, ARF distinguishes itself by the disappearance of the infiltrate when regeneration is complete. The existence of a regenerative potential provided by the network of inflammatory mononuclear leukocytes is supported by studies on tissue repair in different fields. This review discusses the infiltrating network of mononuclear leukocytes as a major participant in the regeneration process after acute renal failure, including the approach which can be followed to investigate this hypothesis.
引用
收藏
页码:355 / 375
页数:21
相关论文
共 105 条
  • [11] SPECIFICITY OF FC-RECEPTORS FOR IGG2A, IGG1-IGG2B, AND IGE ON RAT MACROPHAGES
    BOLTZNITULESCU, G
    BAZIN, H
    SPIEGELBERG, HL
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1981, 154 (02) : 374 - 384
  • [12] MECHANISMS OF ISCHEMIC ACUTE-RENAL-FAILURE
    BONVENTRE, JV
    [J]. KIDNEY INTERNATIONAL, 1993, 43 (05) : 1160 - 1178
  • [13] BORDER WA, 1994, NEW ENGL J MED, V331, P1286
  • [14] CHARACTERIZATION OF MONONUCLEAR CELL SUBSETS IN RENAL CELLULAR INTERSTITIAL INFILTRATES
    BOUCHER, A
    DROZ, D
    ADAFER, E
    NOEL, LH
    [J]. KIDNEY INTERNATIONAL, 1986, 29 (05) : 1043 - 1049
  • [15] BREZIS M, 1991, KIDNEY, P993
  • [16] CALDWELL MD, 1990, J TRAUMA, V30, pS116
  • [17] GENETIC-MAPPING OF THE ATHYMIC NUDE (RNU) LOCUS IN THE RAT TO A REGION CHROMOSOME-10
    CASH, JM
    REMMERS, EF
    GOLDMUNTZ, EA
    CROFFORD, LJ
    ZHA, HB
    HANSEN, CT
    WILDER, RL
    [J]. MAMMALIAN GENOME, 1993, 4 (01) : 37 - 42
  • [18] ANTIGENIC MODULATION - A MAJOR MECHANISM OF ANTIBODY ACTION
    CHATENOUD, L
    BACH, JF
    [J]. IMMUNOLOGY TODAY, 1984, 5 (01): : 20 - 25
  • [19] THERAPY WITH MONOCLONAL-ANTIBODIES BY ELIMINATION OF T-CELL SUBSETS INVIVO
    COBBOLD, SP
    JAYASURIYA, A
    NASH, A
    PROSPERO, TD
    WALDMANN, H
    [J]. NATURE, 1984, 312 (5994) : 548 - 551
  • [20] EPIDERMAL GROWTH-FACTOR ACCELERATES RENAL REPAIR IN MERCURIC-CHLORIDE NEPHROTOXICITY
    COIMBRA, TM
    CIESLINSKI, DA
    HUMES, HD
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (03): : F438 - F443